eff Cancer Research Results
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Power to enhance an anti cancer effect
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Scientific Papers found: Click to Expand⟱
toxicity↑, 3-Bromopyruvate (3BP), a small alkylating
agent, acts as an anti-metabolite to vital substrates in cancer metabolism and exhibits antitumor activity
across various cancer types, but the unformulated 3BP can cause high toxicity
eff↝, This study explores the efficacy of the 3BP clinical derivative KAT/3BP, currently in phase 1 for patients with hepatocellular carcinoma, in lymphoma models.
eff↑, AT/3BP exhibited synergistic activity when combined with lymphoma therapies, including bendamustine and R-CHOP.
Glycolysis↓, At acidic extracellular pH, 3BP enters cancer cells via monocarboxylic acid-1 (MCT-1) and inhibits glycolysis
through hexokinase II (HK-2) covalent modification
HK2↓, with HK-2 inhibition and dissociation from mitochondria, apoptosis-inducing factor (AIF) release, and apoptosis induction (9).
AIF↑,
Apoptosis↑,
NK cell↑, In the latter, tumor growth was in vivo reversed, with an increase in the number of circulating CD4+, CD8+, and NK-
cells
toxicity↑, unformulated 3BP administrations are associated with severe toxicities, including deaths (22,23)
toxicity↓, However, improvements have been made in developing novel 3BP formulations based on
liposomes, polyethylene glycol (PEG), PEGylated liposomes (stealth liposomes), perillyl alcohol
formulations, and others (12,22,24
Dose↝, KAT-101 and KAT-201 are two clinical 3BP derivatives formulated for oral or intratumoral (IT) administration, respectively (National Cancer Institute Thesaurus Codes C193479 and
C193479), now entering the early clinical evaluation of patients with h
AntiTum↑, KAT/3BP has in vivo antitumor activity in a syngeneic mouse model.
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Glycolysis↓, we found that 5-ALA, a natural precursor of heme, can hinder cell glycolysis, which is the main path of energy production for most cancer cells.
LDH↓, ore specifically, we found that 5-ALA can block an enzyme involved in glycolysis, called lactate dehydrogenase (LDH)
eff↝, We found that 5-ALA has a potency of LDH inhibition comparable to other established LDH inhibitors, such as oxamate or tartronic acid
ECAR↓, a marked decrease in extracellular acidification rate (ECAR) was registered as a consequence of administering 5-ALA,
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*cardioP↑, Epidemiological studies associate regular, moderate intake of blueberries and/or anthocyanins with reduced risk of cardiovascular disease, death, and type 2 diabetes, and with improved weight maintenance and neuroprotection.
*neuroP↑,
*Inflam↓, Among the more important healthful aspects of blueberries are their anti-inflammatory and antioxidant actions and their beneficial effects on vascular and glucoregulatory function
*antiOx↓,
*GutMicro↑, Blueberry phytochemicals may affect gastrointestinal microflora and contribute to host health
*Half-Life↑, However, >50% of the 13C still remained in the body after 48 h
*LDL↓, controlled study of 58 diabetic patients, blueberry intake led to a decline in LDL cholesterol, triglycerides, and adiponectin and an increase in HDL cholesterol
*adiP↓,
*HDL↑,
*CRP↓, reduction was documented in inflammatory markers, including serum high-sensitivity C-reactive protein, soluble vascular adhesion molecule-1, and plasma IL-1β
*IL1β↓,
*Risk↓, lower Parkinson disease risk was associated with the highest quintile of anthocyanin (RR: 0.76) and berry (RR: 0.77) intake
*Risk↓, Nurse's Health Study, greater intake of blueberries and strawberries was associated with slower rates of cognitive decline in older adults, with an estimated delay in decline of about 2.5 y
*cognitive↑, Cognitive performance in elderly adults improved after 12 wk of daily intake of blueberry (94) or Concord grape (95) juice.
*memory↑, Better task switching and reduced interference in memory was found in healthy older adults after 90 d of blueberry supplementation
*other↑, After 12 wk of blueberry consumption, greater brain activity was detected using magnetic resonance imaging in healthy older adults during a cognitive challenge.
*BOLD↑, Similarly, during a memory test, regional blood oxygen level-dependent activity detected by MRI (99) was enhanced in the subjects taking blueberry, but not in those taking placebo.
*NO↓, 50–200 mg/d bilberry showed a dose-dependent decrease in neurotoxic NO and malondialdehyde, combined with an increase in neuroprotective antioxidant capacity due to glutathione, vitamin C, superoxide dismutase, and glutathione peroxidase
*MDA↓,
*GSH↑,
*VitC↑,
*SOD↑,
*GPx↑,
*eff↓, The percentage loss of blueberry anthocyanins during −18°C storage was 12% after 10 mo of storage
*eff↓, Freeze-dried blueberry powder loses anthocyanins in a temperature-dependent manner with a half-life of 139, 39, and 12 d when stored at 25, 42, and 60°C, respectively
*eff↓, Blueberries are low in ascorbic acid and high in anthocyanins (187), and notably anthocyanins are readily degraded by ascorbic acid
*eff↝, Shelf-stable blueberry products like jam (196), juice (197), and extracts (198) can lose polyphenolic compounds when stored at ambient temperature whereas refrigeration mitigates losses.
*Risk↓, It can be safely stated that daily moderate intake (50 mg anthocyanins, one-third cup of blueberries) can mitigate the risk of diseases and conditions of major socioeconomic importance in the Western world.
TrxR↓, Gold derivatives are irreversible inhibitors of TrxR. Among them, auranofin (AF), a selective TrxR inhibitor, has proven its effectiveness as a drug for the treatment of rheumatoid arthritis
BioAv↓, further clinical application of AF could be challenging due to the low solubility and insufficient delivery to glioblastoma.
ROS↑, The inhibition of TrxR1, which leads to increased ROS levels, is currently recognized as the primary mechanism of AF cytotoxicity [106]. In vitro studies have also shown that AF inhibits other thioredoxin reductases, such as TrxR2 and TrxR3
eff↝, The literature indicates that not all cancer tumors exhibit the same level of TrxR expression, affecting their sensitivity to AF.
TET1?, AF was shown to inhibit TET1 in T-ALL models
BioAv↑, Encapsulating AF into nanoparticles or combining it with other pharmaceutical excipients can minimize its potential adverse effects, preserve its interaction with serum proteins, and result in greater stability.
TrxR↓, Auranofin (AF) is an FDA-approved antirheumatic drug with anticancer properties that acts as a thioredoxin reductase 1 (TrxR) inhibitor.
AntiCan↓,
GPx4↓, Although functionally AF appeared a potent inhibitor of GPX4 in all NCI–H1299 cell lines, the induction of lipid peroxidation and consequently ferroptosis was limited to the p53 R273H expressing cells.
DNAdam↑, AF mainly induced large-scale DNA damage and replication stress, leading to the induction of apoptotic cell death rather than ferroptosis.
toxicity↓, AF is an orally available, lipophilic, organogold compound with a well-known safety profile that was approved by the U.S. Food and Drug Administration (FDA) for the treatment of rheumatoid arthritis (RA).
eff↝, AF represents a potential novel therapeutic strategy to efficiently kill mutant p53 NSCLC tumor cells through distinct immunogenic cell death pathways.
TrxR↓, Auranofin mainly targets the anti-oxidative system catalyzed by thioredoxin reductase (TrxR), which protects the cell from oxidative stress and death in the cytoplasm and the mitochondria.
ROS↑, Inhibiting TrxR dysregulates the intracellular redox state causing increased intracellular reactive oxygen species levels, and stimulates cellular demise
eff↑, TrxR is over-expressed in many cancers as an adaptive mechanism for cancer cell proliferation, rendering it an attractive target for cancer therapy, and auranofin as a potential therapeutic agent for cancer.
Apoptosis↑, promotion of ASK-induced apoptosis, and blockage of cell growth, proliferation, and survival due to reduced AKT activity and NF-kB- and p53-mediated transcription.
TumCG↓,
TumCP↓,
Akt↓,
NF-kB↓,
DNAdam↑, DNA damage
eff↝, auranofin inhibits TrxR1 in a p53-independent manner
eff↓, Pre-treatment with NAC counteracted the cancer cell killing effects of auranofin,
PI3K↓, auranofin induces cytotoxicity in human pancreatic adenocarcinoma and non-small cell lung cancer via the inhibition of the PI3K/AKT/mTOR pathway
Akt↓,
mTOR↓,
Hif1a↓, auranofin inhibits the cancer cell response to hypoxia, demonstrated by a decrease in HIF-1 𝛼 expression and VEGF secretion upon auranofin treatment under hypoxic conditions
VEGF↓,
Casp3↑, auranofin was shown to induce caspase-3-mediated apoptosis in human ovarian carcinoma SKOV-3 cells
CSCs↓,
ATP↓, it was found that auranofin inhibits ABCG2 function by depleting cellular ATP via inhibition of glycolysis [96]
Glycolysis↓,
eff↑, auranofin synergizes with another Trx1 inhibitor, piperlongumine, in killing gastric cancer cells in association with ROS-mediated ER stress response and mitochondrial dysfunction.
eff↑, when the gold complex is combined with either selenite or tellurite [104]
MMP↓, Increased ROS induced by AUR causes decreased membrane potential in the mitochondrial membrane, resulting in a decrease in anti-apoptotic proteins, caspase-dependent cell death, and translocation of apoptosis-inducing factor (AIF)
AIF↑,
toxicity↓, Auranofin is considered safe for human use in treating rheumatoid arthritis; thus, this gold derivative can reach the clinic for other diseases relatively quickly and at a low cost
TrxR↓, accumulate into cancer cells and to selectively target Thioredoxin (TrxR),
eff↝, 2 µM was able to decrease TrxR enzyme activity by about 68%, compared with auranofin, which at the same concentration
ROS↑, cellular production of reactive oxygen species (ROS)
selectivity↑, IC50: ≤4.25 μg/ml for normal and ≤32.5 μg/ml cerival cancer cells
eff↝, in vitro cytotoxicity assessment of the AgNPs has significant correlation with the total protein concentration in treated cells.
other↝, In the present study, silver nanoparticles were biologically synthesized using pure enzyme α-amylase and the other one by using soluble proteins of neem leaf extracts.
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eff↑, large surface area-to-volume ratio, which can be exploited in cancer radiotherapy to locally enhance the radiation dose deposition in tumors
TumCG↓, Treatment with nanoparticles and a single radiation dose of 10 Gy significantly reduces the growth of colorectal tumors
OS↑, increases the survival time as compared to treatment with radiation only
RadioS↑, combine standard-dose radiotherapy with radiosensitizers to enhance the radiation therapy efficacy locally within tumors while sparing adjacent healthy tissues
eff↑, suggested that graphene enhances the cellular uptake when combined with metals in nanocomposites
ROS↑, ROS, the most potent of these free radicals, can travel to and indirectly damage DNA
DNAdam↑,
eff↝, PEGylated GQD-decorated Silver Nanoprisms (pGAgNPs) show better intracellular uptake as compared to PEGylated Silver Nanoprisms (pAgNPs)
Telomerase↓, AgNPs could inhibit telomerase activity and lead to telomere shortening and dysfunction.
eff↝, Overexpression of telomerase attenuated the anticancer activity of AgNPs, whereas downregulation of telomerase activity or dysfunction of the telomere enhanced the cytotoxicity of AgNPs in HeLa cells.
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*Wound Healing↑, unique antimicrobial properties silver nanocrystallites have garnered substantial attention and are used extensively for biomedical applications as an additive to wound dressings, surgical instruments and bone substitute materials.
*eff↝, cytotoxicity was dependent on various factors such as surface charge and coating materials used in the synthesis, particle aggregation, and the cell-type for the different silver nanoparticles that were investigated.
*toxicity↝, uncoated or colloidal silver nanoparticles were found to be the least toxic to both macrophage and lung epithelial cells
*Half-Life↝, Fecal silver began to decline at 12 h for all the AgNPs and was at baseline levels by 48 h.
*toxicity↓, Acute ingestion of AgNP is well-tolerated at high doses, irrespective of size or coating
*Dose↑, The doses utilized in this study (0.1, 1 and 10 mg/kg bw/d) were equivalent to, respectively, 20×, 200× and 2000× the EPA oral reference dose (RfD, 0.005 mg/kg bw/d) for silver
*other↝, Previous estimates of colloidal silver doses associated with clinically evident argyria range between 40× and 700× the oral RfD, although these typically represent repeated exposures
*eff↝, Acute ingestion of AgNP is well-tolerated with concurrent antibiotic administration
*BioAv↓, Oral bioavailability was previously determined as low (4.2%) for a single 10 mg/kg bw dose of 7.9 nm AgNP-citrate in rats
TumCMig↓, 13 nm AgNPs significantly inhibit the migration and invasiveness of lung adenocarcinoma A549 cells, induce elevated reactive oxygen species and lead to NF-κB directed cellular apoptosis
TumCI↓,
ROS↑,
p‑NF-kB↑, 13 nm AgNPs was able to significantly upregulate the phosphorylation of NF-κB (p-NF-κB) in A549 cells
selectivity↑, we speculate that, AgNPs, which are pointed out that have a sustained release of Ag+ in an environment with lower pH (such as cancer cells)
eff↝, and this inhibitive effect is most pronounced treated with 13 nm AgNPs, while the effect starts decreasing with the size of 45 nm and completely vanishes for 92 nm AgNPs.
*DNAdam↑, AgNPs induced 8-oxoG, double strand breaks (DSBs), chromosomal damage, and DNA deletions in both genotypes
*toxicity↝, In summary, citrate-coated AgNPs are genotoxic in both genotypes and Ogg1 deficiency exacerbates the effect ( 4 mg/kg of citrate-coated AgNPs over a period of 7 d.)
eff↝, data suggest that humans with genetic polymorphisms and mutations in OGG1 may have increased susceptibility to AgNP-mediated DNA damage.
eff↝, AgNPs synthesized are stable up to 10 days without silver and glucose dissolution.
TumCCA↑, AgNPs block the cells in S and G2/M phases, and increase the subG1 cell population.
eff↑, HeLa cells take up abundantly and rapidly AgNPs-G resulting toxic to cells in amount and incubation time dependent manner.
eff↑, The dissolution experiments demonstrated that the observed effects were due only to AgNPs-G since glucose capping prevents Ag+ release.
ROS↑, AgNPs cause toxic responses via induction of oxidative stress as consequence of the generation of intracellular (ROS), depletion of glutathione (GSH), reduction of the superoxide dismutase (SOD) enzyme activity, and increased lipid peroxidation
GSH↓,
SOD↓,
lipid-P↑,
LDH↑, significant LDH levels increase with the highest amount of AgNPs-G and maximum of toxicity was seen at 12 h.
Dose↝, Values found were between 3.2 and 3.9 molecules sugar/nm2.
eff↑, glucose and citrate coated nanoparticles show a similar toxicity, galactose and mannose functionalized nanoparticles were significant less toxic towards both cell lines.
ROS↑, suggesting that the toxicity is mainly caused by oxidative stress related to ROS formation
eff↝, Many authors have argued that in fact the toxicity of nanosilver is only caused by the ionic form [24]
eff↑, Trojan-horse mechanism has been often discussed in literature as a responsible for toxicity of silver nanoparticles.
eff↝, although mannose and glucose-functionalized nanoparticles present similar cellular uptakes, observed toxicities were considerably different.
eff↑, Actually, in this study, glucose-capped nanoparticles present the highest toxicity as well as protein carbonylation, despite their moderate cellular uptake, compared with other nanoparticles.
eff↝, Observed toxicity was strongly correlated with intracellular oxidative stress, measured as protein carbonylation, but not to cellular uptake.
*cachexia↓, The results of this process favored L-carnitine supplementation in patients with cancer-related cachexia.
*Apoptosis↓, inhibiting apoptosis or reversing inflammatory processes.
*Inflam↓,
QoL↑, This treatment increased plasma-free carnitine concentrations and significantly improved fatigue, which was assessed using the functional assessment of cancer therapy, fatigue, and quality of life questionnaire, as well as quality-of-life measu
Dose↝, placebo-controlled trial, in which 2 g per day of LC was administrated orally for four weeks among eligible patients.
Weight↑, advanced pancreatic cancer received either LC (4 g/day orally) or a placebo for 12 weeks. The results showed that body mass index, nutritional status (body cell mass and body fat), and quality-of-life parameters increased
OS↝, There was an insignificant increase in overall survival, a decline in length of hospital stays, and decrease in fatigue among the LC-treated patients.
fatigue↓,
eff↝, some dietary factors, such as food intake restriction and intake of LC and certain micronutrients (vitamin C, vitamin B6, and iron, which are required as cofactors for endogenous LC biosynthesis) may have some effects on the efficacy of LC sup
EGFR↓, Aumolertinib is a well-tolerated third-generation epidermal growth factor receptor tyrosine kinase inhibitor that could serve as a treatment option for EGFR-mutant NSCLC in the first-line setting.
eff↝, Objective response rate and disease control rate were similar in the aumolertinib and gefitinib groups (objective response rate, 73.8% and 72.1%, respectively;
OS↑, see figure 1
*antiOx↑, Apigenin (4′, 5, 7-trihydroxyflavone), a major plant flavone, possessing antioxidant, anti-inflammatory, and anticancer properties
*Inflam↓,
AntiCan↑,
ChemoSen↑, Studies demonstrate that apigenin retain potent therapeutic properties alone and/or increases the efficacy of several chemotherapeutic drugs in combination on a variety of human cancers.
BioEnh↑, Apigenin’s anticancer effects could also be due to its differential effects in causing minimal toxicity to normal cells with delayed plasma clearance and slow decomposition in liver increasing the systemic bioavailability in pharmacokinetic studies.
chemoPv↑, apigenin highlighting its potential activity as a chemopreventive and therapeutic agent.
IL6↓, In taxol-resistant ovarian cancer cells, apigenin caused down regulation of TAM family of tyrosine kinase receptors and also caused inhibition of IL-6/STAT3 axis, thereby attenuating proliferation.
STAT3↓,
NF-kB↓, apigenin treatment effectively inhibited NF-κB activation, scavenged free radicals, and stimulated MUC-2 secretion
IL8↓, interleukin (IL)-6, and IL-8
eff↝, The anti-proliferative effects of apigenin was significantly higher in breast cancer cells over-expressing HER2/neu but was much less efficacious in restricting the growth of cell lines expressing HER2/neu at basal levels
Akt↓, Apigenin interferes in the cell survival pathway by inhibiting Akt function by directly blocking PI3K activity
PI3K↓,
HER2/EBBR2↓, apigenin administration led to the depletion of HER2/neu protein in vivo
cycD1/CCND1↓, Apigenin treatment in breast cancer cells also results in decreased expression of cyclin D1, D3, and cdk4 and increased quantities of p27 protein
CycD3↓,
p27↑,
FOXO3↑, In triple-negative breast cancer cells, apigenin induces apoptosis by inhibiting the PI3K/Akt pathway thereby increasing FOXO3a expression
STAT3↓, In addition, apigenin also down-regulated STAT3 target genes MMP-2, MMP-9, VEGF and Twist1, which are involved in cell migration and invasion of breast cancer cells [
MMP2↓,
MMP9↓,
VEGF↓, Apigenin acts on the HIF-1 binding site, which decreases HIF-1α, but not the HIF-1β subunit, thereby inhibiting VEGF.
Twist↓,
MMP↓, Apigenin treatment of HGC-27 and SGC-7901 gastric cancer cells resulted in the inhibition of proliferation followed by mitochondrial depolarization resulting in apoptosis
ROS↑, Further studies revealed apigenin-induced apoptosis in hepatoma tumor cells by utilizing ROS generated through the activation of the NADPH oxidase
NADPH↑,
NRF2↓, Apigenin significantly sensitized doxorubicin-resistant BEL-7402 (BEL-7402/ADM) cells to doxorubicin (ADM) and increased the intracellular concentration of ADM by reducing Nrf2-
SOD↓, In human cervical epithelial carcinoma HeLa cells combination of apigenin and paclitaxel significantly increased inhibition of cell proliferation, suppressing the activity of SOD, inducing ROS accumulation leading to apoptosis by activation of caspas
COX2↓, melanoma skin cancer model where apigenin inhibited COX-2 that promotes proliferation and tumorigenesis
p38↑, Additionally, it was shown that apigenin treatment in a late phase involves the activation of p38 and PKCδ to modulate Hsp27, thus leading to apoptosis
Telomerase↓, apigenin inhibits cell growth and diminishes telomerase activity in human-derived leukemia cells
HDAC↓, demonstrated the role of apigenin as a histone deacetylase inhibitor. As such, apigenin acts on HDAC1 and HDAC3
HDAC1↓,
HDAC3↓,
Hif1a↓, Apigenin acts on the HIF-1 binding site, which decreases HIF-1α, but not the HIF-1β subunit, thereby inhibiting VEGF.
angioG↓, Moreover, apigenin was found to inhibit angiogenesis, as suggested by decreased HIF-1α and VEGF expression in cancer cells
uPA↓, Furthermore, apigenin intake resulted in marked inhibition of p-Akt, p-ERK1/2, VEGF, uPA, MMP-2 and MMP-9, corresponding with tumor growth and metastasis inhibition in TRAMP mice
Ca+2↑, Neuroblastoma SH-SY5Y cells treated with apigenin led to induction of apoptosis, accompanied by higher levels of intracellular free [Ca(2+)] and shift in Bax:Bcl-2 ratio in favor of apoptosis, cytochrome c release, followed by activation casp-9, 12
Bax:Bcl2↑,
Cyt‑c↑,
Casp9↑,
Casp12↑,
Casp3↑, Apigenin also augmented caspase-3 activity and PARP cleavage
cl‑PARP↑,
E-cadherin↑, Apigenin treatment resulted in higher levels of E-cadherin and reduced levels of nuclear β-catenin, c-Myc, and cyclin D1 in the prostates of TRAMP mice.
β-catenin/ZEB1↓,
cMyc↓,
CDK4↓, apigenin exposure led to decreased levels of cell cycle regulatory proteins including cyclin D1, D2 and E and their regulatory partners CDK2, 4, and 6
CDK2↓,
CDK6↓,
IGF-1↓, A reduction in the IGF-1 and increase in IGFBP-3 levels in the serum and the dorsolateral prostate was observed in apigenin-treated mice.
CK2↓, benefits of apigenin as a CK2 inhibitor in the treatment of human cervical cancer by targeting cancer stem cells
CSCs↓,
FAK↓, Apigenin inhibited the tobacco-derived carcinogen-mediated cell proliferation and migration involving the β-AR and its downstream signals FAK and ERK activation
Gli↓, Apigenin inhibited the self-renewal capacity of SKOV3 sphere-forming cells (SFC) by downregulating Gli1 regulated by CK2α
GLUT1↓, Apigenin induces apoptosis and slows cell growth through metabolic and oxidative stress as a consequence of the down-regulation of glucose transporter 1 (GLUT1).
ChemoSen↑, Apigenin has also been studied for its potential as a sensitizer in cancer therapy, improving the efficacy of traditional chemotherapeutic drugs and radiotherapy
RadioS↑, Apigenin enhances radiotherapy effects by sensitizing cancer cells to radiation-induced cell death
eff↝, It works by suppressing the expression of involucrin (hINV), a hallmark of keratinocyte development. Apigenin inhibits the rise in hINV expression caused by differentiating agents
DR5↑, Apigenin also greatly upregulates the expression of death receptor 5 (DR5
selectivity↑, Surprisingly, apigenin-mediated increase of DR5 expression is missing in normal mononuclear cells from human peripheral blood and doesn't subject these cells to TRAIL-induced death.
angioG↓, Apigenin has been found to prevent angiogenesis by targeting critical signaling pathways involved in blood vessel creation.
selectivity↑, Importantly, apigenin has been demonstrated to selectively kill cancer cells while sparing normal ones
chemoP↑, This selective cytotoxicity is beneficial in cancer therapy because it reduces the negative effects frequently associated with traditional treatments like chemotherapy
MAPK↓, Apigenin's ability to suppress MAPK signaling adds to its anticancer properties.
PI3K↓, Apigenin suppresses the PI3K/Akt/mTOR pathway, which is typically dysregulated in cancer.
Akt↓,
mTOR↓,
Wnt↓, Apigenin inhibits Wnt signaling by increasing β-catenin degradation
β-catenin/ZEB1↓,
GLUT1↓, fig 3
radioP↑, while reducing radiation-induced damage to healthy tissues
BioAv↓, obstacles associated with apigenin's low bioavailability and stability
chemoPv↑, Especially as a chemopreventive agent for cancer
*cognitive↑, The most notable cognitive and mood effects were improved memory performance and increased 'calmness' at all postdose time points for the highest (1600 mg) dose.
*memory↑,
*AChE∅, However, no cholinesterase inhibitory properties were detected
*Mood↑,
*eff↝, The results also suggest that different preparations derived from the same plant species may exhibit different properties depending on the process used for the sample preparation.
AntiCan↑, antimalarial drug, artemisinin that has shown anticancer activities in vitro and in vivo.
toxicity↑, safety of artemisinins in long-term cancer therapy requires further investigation.
Ferroptosis↑, Artemisinins acts against cancer cells via various pathways such as inducing apoptosis (Zhu et al., 2014; Zuo et al., 2014) and ferroptosis via the generation of reactive oxygen species (ROS) (Zhu et al., 2021) and causing cell cycle arrest
ROS↑,
TumCCA↑,
BioAv↝, absolute bioavailability was estimated to be 21.6%. ART has good solubility and is not lipophilic
eff↝, ART would not distribute well to the tissues and might be more effective in treating cancers such as leukemia, hepatocellular carcinoma (HCC), or renal cell carcinoma because the liver and kidney are highly perfused organs.
Half-Life↓, Pharmacokinetic studies showed a relatively short t1/2 of artemisinins. For ART, t1/2 was 0.41 h
Ferritin↓, Figure 3
GPx4↓,
NADPH↓,
GSH↓,
BAX↑,
Cyt‑c↑,
cl‑Casp3↑,
VEGF↓, angiogenesis
IL8↓,
COX2↓,
MMP9↓,
E-cadherin↑,
MMP2↓,
NF-kB↓,
p16↑, cell cycle arrest
CDK4↓,
cycD1/CCND1↓,
p62↓, autophagy
LC3II↑,
EMT↓, suppressing EMT and CSCs
CSCs↓,
Wnt↓, Depress Wnt/β-catenin signaling pathway
β-catenin/ZEB1↓,
uPA↓, Inhibit u-PA activity, protein and mRNA expression
TumAuto↑, Emerging evidence suggests that autophagy induction is one of the molecular mechanisms underlying anticancer activity of artemisinins
angioG↓, Inhibition of Angiogenesis
ChemoSen↑, Many studies also reported that the use of artemisinins sensitized cancer cells to conventional chemotherapy and exerted a synergistic effect on apoptosis, inhibition of cell growth, and a reduction of cell viability, leading to a lower IC50 value
Ferritin↓, dihydroartemisinin (DAT, which triggers lysosomal ferritin degradation).
Iron↑, DAT has shown promise in reversing carboplatin resistance in ovarian cancer cell lines by expanding the labile iron pool (LIP) and enhancing Fenton reaction-mediated lipid peroxidation (149).
Fenton↑,
lipid-P↑,
ChemoSen↑, Its advantage lies in synergistic effects with conventional chemotherapies, as iron overload amplifies chemotherapy-induced oxidative stress.
ROS↑,
eff↝, However, DAT requires careful monitoring of systemic iron levels to avoid anemia, and its efficacy is reduced in cancer cells with upregulated ferroportin (an iron export protein).
toxicity↓, Some sedation, ptosis and ataxia were observed in Sprague-Dawley rats 15–20 minutes of administering a herbal concoction that contained WS at a large dose of 1–2 g/kg body weight [36]
TumW↓, Induction of apoptosis by WA has been noted in some in vivo models where treatment with 4 mg/kg WA, i.p. 5 times for 2 weeks markedly reduced MDA-MB-231 tumor weights in nude mice as well as increased apoptosis compared to tumors in control mice [56
Dose?, 20 mg/kg, oral 3X/wk for 14 wk Hamster Head and Neck Example
eff↝, showed that this chemopreventive capacity was dependent on a circadian pattern where hamsters dosed with WA at 8 AM and 12 PM showed 100% protection from oral tumor formation while those treated at 12 AM showed 50% incidence in oral tumors
Ki-67↓, WA treatment resulted in retarded tumor growth; reduction in cell proliferation marker Ki-67, survivin, and XIAP,
survivin↓,
XIAP↓,
PERK↑, higher protein expression of pERK, pRSK, CHOP and DR-5 was also observed in the WA-treated group compared to control.
p‑RSK↑,
CHOP↑,
DR5↑,
Dose↝, Clinically diagnosed schizophrenia patients who had received antipsychotic medications for 6 months or more received either a capsule with 400 mg of WS extract (n=15), three times daily, for 1 month [80]
BG↓, Results after one month showed significant reduction in serum triglycerides and fasting blood glucose levels in the WS extract- treated group compared to the placebo
DNMTs↓, in MCF7 and MDA-MB-231 breast cancer cells WA treatment suppressed transcription of DNMT.
AntiCan↑, Aloe-emodin possesses multiple anti-proliferative and anti-carcinogenic properties in a host of human cancer cell lines, with often multiple vital pathways affected by the same molecule.
eff↝, The effects of aloe-emodin are not ubiquitous across all cell lines but depend on cell type.
TumCP↓, most notable effects include inhibition of cell proliferation, migration, and invasion; cycle arrest; induction of cell death;
TumCMig↓,
TumCI↓,
TumCCA↑,
TumCD↑,
MMP↓, mitochondrial membrane and redox perturbations; and modulation of immune signaling.
ROS↑, which coincide with deleterious effects on mitochondrial membrane permea-bility and/or oxidative stress via exacerbated ROS production.
Apoptosis↑, In bladder cancer cells (T24), aloe-emodin induced time-and dose-dependent apoptosis [7]
CDK1↓, reduced levels of cyclin-dependent kinase (CDK) 1, cyclin B1, and BCL-2 after treatment with aloe-emodin.
CycB/CCNB1↓,
Bcl-2↓,
PCNA↓, Increases in cyclin B1, CDK1, and alkaline phosphatase (ALP) activity were observed along with inhibition of proliferating cell nuclear antigen (PCNA), showing decreased proliferation.
ATP↓, human lung non-small cell car¬cinoma (H460). They found a time- de¬pendent reduction in ATP, lower ATP synthase expression
ER Stress↑, hypothesized to cause apoptosis by augmenting endoplasmic reticulum stress [16].
cl‑Casp3↑, (HepG2) cells underwent apoptosis through a cas-pase-dependent pathway with cleavage and activation of caspases-3/9 and cleavage of PARP [24]
cl‑Casp9↑,
cl‑PARP↑,
MMP2↓, Matrix metalloproteinase-2 was significantly decreased, with an increase in ROS and cytosolic calcium.
Ca+2↑,
DNAdam↑, U87 malignant glioma cells through disruption of mitochondrial membrane potential, cell cycle arrest in the S phase, and DNA fragmentation in a time-dependent manner with minimal necrosis
Akt↓, Prostate cancer. Following treatment with aloe-emodin, mTORC2's down¬stream enzymes, AKT and PKCa, were inhibited
PKCδ↓,
mTORC2↓, Proliferation of PC3 cells was inhibited as a result of aloe-emodin binding to mTORC2, with inhibition of mTORC2 kinase activity.
GSH↓, Skin cancer. Intracellular ROS increased, while intra-cellular-reduced glutathione (GSH) was depleted and BCL-2 (anti-apoptotic protein) was down-regulated.
ChemoSen↑, Aloe-emodin also sensitizes skin cancer cells to chemo-therapy. aloe-emodin and emodin potentiated the therapeutic effects of cisplatin, doxo-rubicin, 5-fluorouracil
*BioAv↑, β-glucan is a relatively inexpensive milling byproduct, and it is added to foods on the assumption that this will contribute to health benefits.
*toxicity↓, Moreover, no human adverse effects have been reported following the consumption of a diet rich in β-glucan from oat or barley flour or their extracts [70].
*Imm↑, Among polysaccharides that act as immunostimulants, β-glucans were found to be the most effective against infectious diseases and cancer [88].
*eff↑, The immunological potency of β-glucans varies with the molecular mass, solution conformation, backbone structure, degree of branching as well as the cell type that is targeted [89].
*Risk↓, pretreatment of high-risk surgical patients with intravenous yeast β-(1,3; 1,6)-D-glucan decreased the infection incidence, shortened intensive care unit length stay, and improved survival in comparison to a saline placebo injection
*Weight↓, In this particular study, chitin-glucan decreased high fat diet-induced body weight gain, fat mass development, fasting hyperglycemia, glucose intolerance,
*eff↝, A drink containing 5 g of oat β-glucan with a molecular weight 70 000 Da significantly lowered postprandial glucose and insulin levels relative to a rice drink control, while a similar drink containing barley β-glucan 40 000 Da had no effect
*BP↓, 8 g/day of supplemented soluble fiber from oat bran over 12 weeks significantly reduced both systolic and diastolic blood pressure in comparison to the control [197].
*GutMicro↑, Beta glucans selectively support the growth of Lactobacilli and Bifidobacteria, both of them being antagonists to pathogenic bacteria in the digestive system [
*eff↓, freeze-thaw cycle reduced the solubility of β-glucan in oat bran muffins by 9% to 55% of the fresh values.
SOD1↑, Baicalein ONLY: increase in the expression of the SOD1 , SOD2 and GPX1 genes compared to the nontreated cell cultures
SOD2↑,
GPx1↑,
Dose?, A chamber with a field induction of 0.7 T was used for the tests
eff↝, There was no significant difference in the expression of the SOD1, SOD2 or GPX1 genes in the melanoma cell cultures that had only been exposed to a static magnetic field (0.7 T)
SOD1↓, Baicalein + 0.7T MF: decreases SOD1 , SOD2 and GPX1
SOD2↓,
GPx1↓,
*Inflam↓, BBR exerts remarkable anti-inflammatory (94–96), antiviral (97), antioxidant (98), antidiabetic (99), immunosuppressive (100), cardiovascular (101, 102), and neuroprotective (103) activities.
*antiOx↑,
*cardioP↑,
*neuroP↑,
TumCCA↑, BBR could induce G1 cycle arrest in A549 lung cancer cells by decreasing the levels of cyclin D1 and cyclin E1
cycD1/CCND1↓,
cycE/CCNE↓,
CDC2↓, BBR also induced G1 cycle arrest by inhibiting cyclin B1 expression and CDC2 kinase in some cancer cells
AMPK↝, BBR has been suggested to induce autophagy in glioblastoma by targeting the AMP-activated protein kinase (AMPK)/mechanistic target of rapamycin (mTOR)/ULK1 pathway
mTOR↝,
Casp8↑, BBR has been revealed to stimulate apoptosis in leukemia by upregulation of caspase-8 and caspase-9
Casp9↑,
Cyt‑c↑, in skin squamous cell carcinoma A431 cells by increasing cytochrome C levels
TumCMig↓, BBR has been confirmed to inhibit cell migration and invasion by inhibiting the expression of epithelial–mesenchymal transition (EMT)
TumCI↓,
EMT↓,
MMPs↓, metastasis-related proteins, such as matrix metalloproteinases (MMPs) and E-cadherin,
E-cadherin↓,
Telomerase↓, BBR has shown antitumor effects by interacting with microRNAs (125) and inhibiting telomerase activity
*toxicity↓, Numerous studies have revealed that BBR is a safe and effective treatment for CRC
GRP78/BiP↓, Downregulates GRP78
EGFR↓, Downregulates EGFR
CDK4↓, downregulates CDK4, TERT, and TERC
COX2↓, Reduces levels of COX-2/PGE2, phosphorylation of JAK2 and STAT3, and expression of MMP-2/-9.
PGE2↓,
p‑JAK2↓,
p‑STAT3↓,
MMP2↓,
MMP9↓,
GutMicro↑, BBR can inhibit tumor growth through meditation of the intestinal flora and mucosal barrier, and generally and ultimately improve weight loss. BBR has been reported to modulate the composition of intestinal flora and significantly reduce flora divers
eff↝, BBR can regulate the activity of P-glycoprotein (P-gp), and potential drug-drug interactions (DDIs) are observed when BBR is coadministered with P-gp substrates
*BioAv↓, the efficiency of BBR is limited by its low bioavailability due to its poor absorption rate in the gut, low solubility in water, and fast metabolism. Studies have shown that the oral bioavailability of BBR is 0.68% in rats
BioAv↑, combining it with p-gp inhibitors (such as tariquidar and tetrandrine) (196, 198), and modification to berberine organic acid salts (BOAs)
Inflam↓, BBR has documented to have anti-diabetic, anti-inflammatory and anti-microbial (both anti-bacterial and anti-fungal) properties.
IL6↓, BBRs can inhibit IL-6, TNF-alpha, monocyte chemo-attractant protein 1 (MCP1) and COX-2 production and expression.
MCP1↓,
COX2↓,
PGE2↓, BBRs can also effect prostaglandin E2 (PGE2)
MMP2↓, and decrease the expression of key genes involved in metastasis including: MMP2 and MMP9.
MMP9↓,
DNAdam↑, BBR induces double strand DNA breaks and has similar effects as ionizing radiation
eff↝, In some cell types, this response has been reported to be TP53-dependent
Telomerase↓, This positively-charged nitrogen may result in the strong complex formations between BBR and nucleic acids and induce telomerase inhibition and topoisomerase poisoning
Bcl-2↓, BBR have been shown to suppress BCL-2 and expression of other genes by interacting with the TATA-binding protein and the TATA-box in certain gene promoter regions
AMPK↑, BBR has been shown in some studies to localize to the mitochondria and inhibit the electron transport chain and activate AMPK.
ROS↑, targeting the activity of mTOR/S6 and the generation of ROS
MMP↓, BBR has been shown to decrease mitochondrial membrane potential and intracellular ATP levels.
ATP↓,
p‑mTORC1↓, BBR induces AMPK activation and inhibits mTORC1 phosphorylation by suppressing phosphorylation of S6K at Thr 389 and S6 at Ser 240/244
p‑S6K↓,
ERK↓, BBR also suppresses ERK activation in MIA-PaCa-2 cells in response to fetal bovine serum, insulin or neurotensin stimulation
PI3K↓, Activation of AMPK is associated with inhibition of the PI3K/PTEN/Akt/mTORC1 and Raf/MEK/ERK pathways which are associated with cellular proliferation.
PTEN↑, RES was determined to upregulate phosphatase and tensin homolog (PTEN) expression and decrease the expression of activated Akt. In HCT116 cells, PTEN inhibits Akt signaling and proliferation.
Akt↓,
Raf↓,
MEK↓,
Dose↓, The effects of low doses of BBR (300 nM) on MIA-PaCa-2 cells were determined to be dependent on AMPK as knockdown of the alpha1 and alpha2 catalytic subunits of AMPK prevented the inhibitory effects of BBR on mTORC1 and ERK activities and DNA synthes
Dose↑, In contrast, higher doses of BBR inhibited mTORC1 and ERK activities and DNA synthesis by AMPK-independent mechanisms [223,224].
selectivity↑, BBR has been shown to have minimal effects on “normal cells” but has anti-proliferative effects on cancer cells (e.g., breast, liver, CRC cells) [225–227].
TumCCA↑, BBR induces G1 phase arrest in pancreatic cancer cells, while other drugs such as gemcitabine induce S-phase arrest
eff↑, BBR was determined to enhance the effects of epirubicin (EPI) on T24 bladder cancer cells
EGFR↓, In some glioblastoma cells, BBR has been shown to inhibit EGFR signaling by suppression of the Raf/MEK/ERK pathway but not AKT signaling
Glycolysis↓, accompanied by impaired glycolytic capacity.
Dose?, The IC50 for BBR was determined to be 134 micrograms/ml.
p27↑, Increased p27Kip1 and decreased CDK2, CDK4, Cyclin D and Cyclin E were observed.
CDK2↓,
CDK4↓,
cycD1/CCND1↓,
cycE/CCNE↓,
Bax:Bcl2↑, Increased BAX/BCL2 ratio was observed.
Casp3↑, The mitochondrial membrane potential was disrupted and activated caspase 3 and caspases 9 were observed
Casp9↑,
VEGFR2↓, BBR treatment decreased VEGFR, Akt and ERK1,2 activation and the expression of MMP2 and MMP9 [235].
ChemoSen↑, BBR has been shown to increase the anti-tumor effects of tamoxifen (TAM) in both drug-sensitive MCF-7 and drug-resistant MCF-7/TAM cells.
eff↑, The combination of BBR and CUR has been shown to be effective in suppressing the growth of certain breast cancer cell lines.
eff↑, BBR has been shown to synergize with the HSP-90 inhibitor NVP-AUY922 in inducing death of human CRC.
PGE2↓, BBR inhibits COX2 and PEG2 in CRC.
JAK2↓, BBR prevented the invasion and metastasis of CRC cells via inhibiting the COX2/PGE2 and JAK2/STAT3 signaling pathways.
STAT3↓,
CXCR4↓, BBR has been observed to inhibit the expression of the chemokine receptors (CXCR4 and CCR7) at the mRNA level in esophageal cancer cells.
CCR7↓,
uPA↓, BBR has also been shown to induce plasminogen activator inhibitor-1 (PAI-1) and suppress uPA in HCC cells which suppressed their invasiveness and motility.
CSCs↓, BBR has been shown to inhibit stemness, EMT and induce neuronal differentiation in neuroblastoma cells. BBR inhibited the expression of many genes associated with neuronal differentiation
EMT↓,
Diff↓,
CD133↓, BBR also suppressed the expression of many genes associated with cancer stemness such as beta-catenin, CD133, NESTIN, N-MYC, NOTCH and SOX2
Nestin↓,
n-MYC↓,
NOTCH↓,
SOX2↓,
Hif1a↓, BBR inhibited HIF-1alpha and VEGF expression in prostate cancer cells and increased their radio-sensitivity in in vitro as well as in animal studies [290].
VEGF↓,
RadioS↑,
ACLY↓, Bempedoic acid competitively inhibits ACLY activity and allosterically activates AMP-activated protein kinase-β1 (AMPKβ1)-
AMPK↑,
eff↑, unlike bempedoic acid30, EVT0185-CoA inhibited rather than activated AMPKβ1-containing complexes (Extended Data Fig. 5d), and also inhibited ACC1, ACC2 and ACSS2
other↝, Given the role of AMPK in pro-survival signalling38 and the compensatory upregulation of ACSS2 upon ACLY inhibition8,9,12, these findings highlight key mechanistic differences between EVT0185 and bempedoic acid
eff↝, EVT0185 reduced tumour burden, whereas bempedoic acid had limited efficacy
ROS↑, Formation of reactive oxygen species [6], modulation of BCL-2 and BAX levels [8] and topoisomerases Ia and IIa [11] have been suggested to be involved in its mechanisms of action.
Bcl-2↓,
BAX↑,
TOP1↝,
eff↝, betulinic acid was more than ten times less potent than doxorubicin
toxicity↓, Thus on normal PBL betulinic acid was at least 1000-fold less toxic than doxorubicin.
toxicity↓, Mice treated with betulinic acid did not
show any sign of apparent toxicity or body weight loss
compared with controls.
selectivity↑, Moreover, in spite of the lower potency compared with doxorubicin, betulinic acid seems to be selective for tumor cells, since minimal toxicity
against normal cells was observed
Apoptosis↑, BJO induced AML cell apoptosis through activation of caspase-8 and modulation of apoptosis-related proteins.
Casp8↑,
TumCCA↑, BJO also increased subG1 phase cells and cause PARP cleavage in AML patients' leukemia cells.
cl‑PARP↑,
eff↝, Moreover, oleic acid and linoleic acid were found to be the active components of BJO.
TumCG↓, Furthermore, intravenous injection of BJO significantly inhibited U937 tumor growth in the xenograft mouse model.
necrosis↑, BJO induced apoptosis at low concentrations and induced necrosis at higher concentrations
Fas↑, upregulating expression of Fas in leukemia cells
TumCCA↑, BJO can arrest the cell cycle in G0/G1 phase [6, 7] to inhibit cell growth.
selectivity↑, Its apoptotic effect on AML cells was much more potent than on normal PBLs from healthy volunteers.
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Colon, |
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SW-620 |
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AQPs↓, Bacopa monnieri, blocks the AQP1 water channel and impairs migration of cells that express AQP1.
TumCG↓, Bacopaside II significantly reduced growth at ≥20 µM for HT-29 and ≥15 µM for SW480, SW620 and HCT116.
TumCCA↓, These results are the first to show that bacopaside II inhibits colon cancer cell growth by inducing cell cycle arrest and apoptosis.
Apoptosis↑,
eff↝, bacopaside II impaired migration of the high AQP1 expressing HT-29 but had minimal effect on the low expressing SW480,
*eff↓, excessive protein fermentation produces branched-chain fatty acid (BCFA), ammonia, phenols, and other metabolites that inhibit butyrate production
Dose↝, Several studies have found that the ratio of acetate to propionate to butyrate in the colon of healthy individuals (regardless of region) has been found to be approximately 60:20:20 [2,3].
eff↑, An appropriate polysaccharide-to-protein ratio appears crucial for maintaining gut microbial homeostasis and facilitating butyrate generation.
HDAC↓, butyrate is a classic HDAC inhibitor that increases the acetylation level of histone H3 and H4,
ac‑H3↓,
ac‑H4↓,
*HCAR2↑, butyrate is produced by the gut microbiota at high concentrations (10–20 mM) and acts as an endogenous agonist of GPR109A.
*Inflam↓, When butyrate activates GPR109A on colonocytes, it triggers intracellular signaling cascades, promotes the secretion of the anti-inflammatory cytokine IL-18,
*ROS↓, Moreover, butyrate reduces the level of reactive oxygen species by activating the Nrf2 antioxidant pathway and enhancing glutathione (GSH) synthesis, and alleviate stress damage to the to intestinal barrier and immune cells.
*NRF2↑,
*GSH↑,
*CLDN1↑, Butyrate also enhances epithelial barrier function by upregulating the expression of tight junction proteins such as Claudin-1, Occludin, and ZO-1 in intestinal epithelial cells.
*ZO-1↑,
IL1β↓, rucial role in repairing and strengthening the intestinal barrier by downregulating the transcription of pro-inflammatory genes, including IL-1β, IL-6, and COX-2,
IL6↓,
COX2↓,
eff↝, Different types of monosaccharides significantly influence the efficiency of butyrate production due to their distinct chemical properties and microbial utilization mechanisms.
eff↑, After entering the colon, polysaccharides serve as fermentation substrates for gut microbiota and are broken down into butyrate.
other↝, A central challenge in current research on gut microbiota and butyrate production lies in determining the optimal dietary ratio of polysaccharides to proteins.
eff↝, beneficial effects of caffeic acid and ellagic acid were dependent upon the gut microbiota.
eff↑, caffeic acid, ferulic acid, and ellagic acid were also able to significantly ameliorate the severity of colitis, including reduced weight loss, decreased DAI score, relief of colon shortening and lower infiltration of inflammatory cell in the colonic
Weight↑,
Apoptosis↑,
TumCCA↓, CAPE (1-80 uM) can stimulate apoptosis and cell cycle arrest (G1 phase
TumCMig↓,
TumMeta↓,
ChemoSen↑,
eff↑, Nanoparticles promote therapeutic effect of CA and CAPE in reducing cancer cell malignancy.
eff↑, improve capacity of CA and CAPE in cancer suppression, it has been co-administered with other anti-tumor compounds such as gallic acid
eff↓, Currently, solvent extraction is utilized by methanol and ethyl acetate
combination at high temperatures. However, a low amount of CA is
yielded via this pathway
eff↝, Decyl CA (DCA) is a
novel derivative of CA but its role in affecting colorectal cancer has not
been completely understood.
Dose∅, The CAPE administration (0-60 uM) induces both
autophagy and apoptosis in C6 glioma cells.
AMPK↑, CAPE induces autophagy via AMPK upregulation.
p62↓, CAPE can induce autophagy via p62 down-regulation and LC3-II upregulation
LC3II↑,
Ca+2↑, CA (0-1000 uM) enhances Ca2+ accumulation in cells in a concentration-dependent manner
Bax:Bcl2↑, CA can promote Bax/Bcl-2 ratio i
CDK4↑, The administration of CAPE (1–80 μM)
can stimulate apoptosis and cell cycle arrest (G1 phase) via upregulation of Bax, CDK4, CDK6 and Rb
CDK6↑,
RB1↑,
EMT↓, CAPE has demonstrated high potential in inhibiting EMT in nasopharyngeal caner via enhancing E-cadherin levels, and reducing vimentin and β-catenin levels.
E-cadherin↑,
Vim↓,
β-catenin/ZEB1↓,
NF-kB↓,
angioG↑, CAPE (0.01-1ug/ml) inhibited angiogenesis via VEGF down-regulation
VEGF↓,
TSP-1↑, and furthermore, CAPE is capable of increasing TSP-1 levels
MMP9↓, CAPE was found to reduce MMP-9 expression
MMP2↓, CAPE can also down-regulate MMP-2
ChemoSen↑, role of CA and its derivatives in enhancing therapy sensitivity of cancer cells.
eff↑, CA administration (100 uM) alone or its combination with metformin (10 mM) can induce AMPK signaling
ROS↑, CA can promote ROS levels to induce cell death in human squamous cell carcinoma
CSCs↓, CA can reduce self-renewal capacity of CSCs and their migratory ability in vitro and in vivo.
Fas↑, CAPE (0-100 uM) is capable of inducing Fas signaling to promote p53 expression, leading to apoptotic cell death via Bax and caspase activation
P53↑,
BAX↑,
Casp↑,
β-catenin/ZEB1↓, anti-tumor activity of CAPE is mediated via reducing β-catenin levels
NDRG1↑, CAPE (30 uM) can promote NDRG1 expression via MAPK activation and down-regulation of STAT3
STAT3↓,
MAPK↑, CAPE stimulates mitogen-activated protein kinase (MAPK) and ERK
ERK↑,
eff↑, Res, thymoquinone and CAPE mediate lung tumor cell death via Bax
upregulation and Bcl-2 down-regulation.
eff↑, co-administration of CA (100 μM) and
metformin (10 mM) is of interest in cervical squamous cell carcinoma
therapy.
eff↑, in addition to CA, propolis contains other agents such as chrysin, p-coumaric acid and ferulic acid that are beneficial in tumor suppression.
Risk↓, Milk intake was unrelated to rectal cancer risk. High calcium intake had a greater protective effect against tumors of the distal colon and rectal cancer vs. proximal colon
eff↝, The risk reduction associated with calcium was similar for dietary and supplemental sources.
Risk↓, Vitamin D was associated with a nonsignificant 6% reduction in CRC risk.
Risk↓, higher calcium intake was consistently associated with reduced CRC risk across tumor sites and sources of calcium.
Dose↓, Mean (SD) total calcium intake was 401 mg/d (104 mg/d) for females and 407 mg/d (95 mg/d) for males in the lowest quintile (Q1)
eff↝, While our study found an inverse association of total and supplemental calcium intake with rectal cancer risk, we did not observe a statistically significant association with dietary calcium intake.
*Inflam↓, Monoterpenes like thymol and carvacrol are recognized for their anti‐inflammatory and anticancer properties,
AntiCan↑,
PI3K↓, Thymol derivatives, such as 1,2,3‐triazoles and carvacrol, effectively target breast cancer (BC) through PI3K/AKT/mTOR and NOTCH pathways and inhibit PIK3CA expression.
Akt↓,
mTOR↓,
NOTCH↓,
PIK3CA↓,
EGFR↓, thymol exhibits anti‐EGFR activity, while carvacrol modulates the HIF‐1α/VEGF pathway, making them potential candidates for colorectal cancer (CRC) management.
Hif1a↓,
VEGF↓,
ChemoSen↑, Their synergistic potential with chemotherapy, radiotherapy, and other bioactive compounds strengthens their therapeutic promise.
RadioS↑,
eff↝, challenges such as stability, bioavailability, and the need for clinical trials hinder their clinical application.
*cardioP↑, cardioprotective (Joshi et al. 2023), neuroprotective (Forqani et al. 2023) and hepato‐nephroprotective
*neuroP↑,
*hepatoP↑,
Apoptosis↑, Induction of Apoptosis
MMP↓, The apoptosis was due to ROS production, variations in the mitochondrial membrane, caspase‐3 activation, and DNA damage
Casp3↑,
ROS↑,
DNAdam↑,
eff↑, Thymol derivative, known as compound 10 (IC50 6.17 μM) exhibited 3.2‐fold more inhibition than 5‐fluorouracil (IC50 20.09 μM) against MCF‐7
BAX↑, Carvacrol (25, 50, 75, and 90 μM) enhanced the expression of Bax, Bad, Fas‐L, and cytochrome c, activated caspase‐9/3 and caspase‐8, induced cell cycle at G0/G1
BAD↑,
FasL↑,
Cyt‑c↑,
Casp9↑,
Casp8↑,
TumCCA↑,
P21↑, improved the expression of proteins (p21, cyclin D1, CDK4), and downregulated the SMO and GLI1 proteins expression in CC
Smo↓,
Gli1↓,
JNK↑, Moreover, thymol activated JNK and p38 MAPK while impeding the ERK pathway
ERK↓,
MAPK↓, Besides thymol, carvacrol has also been reported to inhibit MAPK or ERK pathways in previous studies.
TRPM7↓, inhibited TRPM7 expression in liver fibrotic C57BL/6J mice
Wnt/(β-catenin)↓, hymol inhibited HCT116 and LoVo cell line invasion via downregulating the Wnt/β‐catenin pathway and reducing c‐Myc and Cyclin D1 expression
BioAv↝, thymol and carvacrol are volatile, and their stability is influenced by these factors (temperature, light, oxygen, and pH)
BioAv↑, Ultrasonication is an effective technique to enhance the stability of thymol and other bioactive compounds. 400 watts of power elevated the performance of NC‐CH formulations, and NC‐CH‐400 displayed increased solubility.
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Arthritis, |
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IBD, |
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AD, |
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Park, |
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*other↝, The most abundant and promising bioactive compound derived from the root of this plant is celastrol, also called tripterine, which possess a broad range of biological activities
*other↝, TW is generally used in the treatment of Crohn’s disease (CD) in China.
*CRP↓, Inflammatory parameters, including c-reactive protein (CRP), also decreased
*eff↝, Etanercept plus TW had an equivalent therapeutic effect to that of Etanercept plus MTX and were both well tolerated
*other↑, TW in human kidney transplantation (26). Rejection occurred in 4.1% of patients treated with TW versus 24.5% of control patients, showing efficacy in the prevention of renal allograph rejection
*CXCR4↓, celastrol decreases hypoxia-induced FLS invasion by inhibiting HIF-1α-mediated CXCR4 transcription
*IL1β↓, Authors have shown that it decreases the production of IL-1β, IL-6, IL-17, IL-18, and TNF by SIC cells harvested from arthritic rats
*IL6↓,
*IL17↓,
*IL18↓,
*TNF-α↓,
*MMP9↓, celastrol reduces MMP-9 production, which limits bone damage
*PGE2↓, celastrol suppresses LPS-induced expression of PEG2 via the downregulation of COX-1 and COX-2 activation
*COX1↓,
*COX2↓,
*PI3K↓, associated with a decrease in PI3K/Akt pathway
*Akt↓,
*other↑, Remarkably, this bone-protective property of celastrol in arthritic models is further supported by studies performed in cancer models
TumCCA↑, celastrol induces cell cycle arrest, apoptosis, and autophagy by the activation of reactive oxygen species (ROS)/c-Jun N-terminal kinases (JNK) signaling pathway
Apoptosis↑,
ROS↑,
JNK↑,
TumAuto↑, celastrol is still able to induce autophagy through HIF/BNIP3 activation
Hif1a↓, The inhibitory effect of celastrol on angiogenesis is mediated by the suppression of HIF-1α,
BNIP3↝,
HSP90↓, The inhibition of HSP90 by celastrol
Fas↑, activation of Fas/Fas ligand pathway in non-small-cell lung cancer
FasL↑,
ETC↓, inhibition of mitochondrial respiratory chain (MRC) complex I
VEGF↓, This inhibition of HIF-1α leads to the decrease of its target genes, such as the VEGF
angioG↓, Angiogenesis Inhibition
RadioS↑, celastrol can overcome tumor resistance to radiotherapy in prostate (129) and lung cancer cells
*neuroP↑, celastrol is a promising neuroprotective agent in animal models of neurodegenerative diseases, such as Parkinson disease (149), Huntington disease (149–151), Alzheimer disease
*HSP70/HSPA5↑, his induction of HSP70 by celastrol explains its beneficial effects not only in neurodegenerative disorders but also in inflammatory diseases.
*ROS↓, celastrol protects human dopaminergic cells from injury and apoptosis and prevents ROS generation and mitochondrial membrane potential loss
*MMP↑,
*Cyt‑c↓, It inhibits cytochrome c release, Bax/Bcl-2 alterations, caspase-9/3 activation, and p38 MAPK activation
*Casp3↓,
*Casp9↓,
*MAPK↓,
*Dose⇅, Authors discuss that it seems to have a narrow therapeutic window, and suggest that it may have a biphasic effect with protective properties at low concentrations and toxic effects at higher concentrations.
*HSPs↑, induces a set of HSPs (HSP27, 32, and 70) in rat cerebral cortical cultures, which are selectively impacted during the progression of this disease
BioAv↓, Due to this poor water solubility, celastrol has low bioavailability. oral administration of celastrol in rats results in ineffective absorption into the systemic circulation, with an absolute bioavailability of 17.06%
Dose↝, narrow therapeutic window of dose together with the occurrence of adverse effects. Our own data showed in vivo that the doses of 2.5 and 5 μg/g/day are effective and non-toxic in the treatment of arthritis in rats;
other↓, During chemotherapy, homocysteine (P = 0.032) and vitamin B12 (P < 0.001) concentrations increased, while folate and platelets decreased (decreases with supplements)
other↝, we also verified a correlation between Hcy levels and cofactors (B12 vitamin and folate).
homoC↓, The anti‐DNA action of alkylating agents would lead to a reduction of folic acid and vitamin B12 concentrations, which in turn would lead to an increase of homocysteine concentration (supplements would lower homoC)
eff↝, As seen in this study, vitamin B12 and folic acid concentrations decreased with the progression of treatment, and they are inversely related to homocysteine levels.
other↝, increase homocysteine concentration 6 months after chemotherapy, as well as a significant decrease in vitamin B12, folic acid, and platelets at the third and sixth month after beginning of chemotherapy treatment in women with BC.
angioG↓, Both chitosan and its various derivatives have been reported to selectively permeate through the cancer cell membranes and show anticancer activity through the cellular enzymatic, antiangiogenic, immunoenhancing, antioxidant defense mechanism, and ap
*Imm↑,
*antiOx↑,
selectivity↑, They get sequestered from noncancer cells and provide their enhanced bioavailability in cancer cells in a sustained release manner.
other↝, The degree of deacetylation (DDA) of chitin ranges from 60 to 100 % and molecular weight of commercially obtained chitosan ranges from 3800 to 20,000 Daltons.
toxicity↓, The degree of deacetylation (DDA) of chitin ranges from 60 to 100 % and molecular weight of commercially obtained chitosan ranges from 3800 to 20,000 Daltons.
BioAv↑,
eff↝, exert anticancer activity with minimal toxicity on noncancer cells [13] and such activity against different cancer cell lines significantly depends upon molecular weight and DDA [
Half-Life↑, Sustained Release Mechanism
MPT↑, Chitosan MDA-MB-231 Permeation enhancement, lowering of MMP9 activity
MMP9↓,
lipid-P↑, induction of lipid peroxidation, enhanced permeation and retention (EPR) effect
EPR↑,
NK cell↑, Immunoenhancement through increase in activity of NK cells, T cells, killer lymphocytes and cytokins.
Casp3↑, Cellular apoptosis, activation of caspase-3 and caspase-8,
Casp8↑,
TumCCA↑, Cytokine signaling cell cycle arrest, ROS activation
ROS↑,
DDS↑, CMCS has been prepared as a carrier of anticancer drug such as 5- fluorouracil, curcumin, and doxorubicin
VEGF↓, decrease in VEGF level and increase in TIMP1 level after 14-day treatment of mouse serum with CMCS in vivo.
TIMP1↑,
ChemoSen↑, The paclitaxel loaded modified glycol chitosan nanoparticles in the size of 400 nm has been found to show sustained release of paclitaxel to bring about the inhibition of MCF-7 tumor growth due to EPR effect in vitro
eff↑, Chitosan-curcumin nanoformulation has been found to show anticancer activity following the apoptotic pathways associated with DNA damage, cell-cycle blockage, and elevation of ROS levels in vivo
chemoP↑, results suggested that CoQ10 provides some protection against cardiotoxicity or liver toxicity during cancer treatment.
cardioP↑,
hepatoP↑,
eff↝, Further investigations are necessary to determine whether CoQ10 can improve the tolerability of cancer treatments.
Ferritin↓, cells treated with curcumin also exhibit a decrease in ferritin, which is consistent with its chemical structure and iron chelating activity.
IronCh↑,
TumAuto↑, curcumin-induced autophagy and apoptosis, together with the tumorigenic action of iron overload.
Apoptosis↑,
eff↝, The assay of intracellular iron showed that iron chelation by curcumin does not alter cellular iron uptake, whereas curcumin only slightly affected the total amount of intracellular iron
Dose↝, interesting to note that there is a huge difference between 10 and 25 μM curcumin treatment and also that cumulated cell death (apoptosis + necrosis) reached 60–70% at 25 μM curcumin with 24-h incubation.
Risk↓, CRMs were well tolerated, and metformin and aspirin showed the most promising effect in reducing cancer risk in a selected group of patients.
AMPK↑, the increased AMP levels activate AMPK
Akt↓, This activation results in the inhibition of AKT and mTOR pathways
mTOR↓,
SIRT1↑, energy deficit also activates the SIRT pathways, which downregulates HIF1α, and the Nrf2 pathway
Hif1a↓,
NRF2↓,
SOD↑, enhances antioxidant defenses (e.g., superoxide dismutase SOD1 and SOD2)
ROS↑, Additionally, in prostate cancer (PC) [55] and triple-negative breast cancer (TNBC) [56] cell lines glucose restriction (GR) has been shown to trigger an increase in ROS, leading to cell death.
IGF-1↓, CR decreases poor prognosis markers such as IGF1, pAKT, and PI3K
p‑Akt↓,
PI3K↑,
GutMicro↑, induces changes in the gut microbiome linked to anti-tumor effects
OS↑, Incorporating a nutraceutical regimen like CR or KD with CT has reduced tumor growth and relapse and improved the survival rate
eff↝, type of dietary intervention, with FMD being the first option, followed by KD and CR last. FMD has been considered the most cost-effective and applicable because it does not completely restrict food intake.
ROS↑, findings consistently indicating that dietary restrictions render highly proliferative tumor cells more susceptible to oxidative damage
TumCCA↑, CR has been reported to induce cell cycle arrest in the G0/G1 phases , enabling cells to undergo DNA repair more efficiently and diminishing DNA damage by CRT
*DNArepair↑,
DNAdam↑, In contrast, tumoral cells, which have an altered cell cycle, are unable to repair DNA, leading to cell death
*toxicity∅, Data suggest overall good compliance, no malnutrition, minimal side effects. No significant changes were identified to suggest increased harm.
QoL∅, unchanged quality of life (QOL),
eff↑, improved endocrine parameters
eff↝, mixed results for cancer outcomes
ChemoSideEff↓, decreasing chemotherapy-related side effects
TumCG↓, limiting tumor growth
Dose↑, When fasting is used as an adjunct to chemotherapy, a minimum fasting period of at least 48 hours is currently recommended for nutritional interventions in order to achieve a measurable metabolic response at the cellular level
toxicity↝, The increased risk for poor outcomes associated with malnutrition, weight loss, and cachexia poses an obvious safety concern for patients with cancer who participate in calorie-restricted fasting
eff↑, short-term fasting involving water-only or limited daily calorie consumption for less than a week has the potential to achieve positive metabolic changes while avoiding malnutrition and significant weight loss
IGF-1↑, statistically significant decrease in IGF-1 among participants compliant with fasting compared with regular diet during the middle of therapy
*OXPHOS↑, Healthy cells also use mitochondrial oxidative phosphorylation for metabolism while cancer cells use aerobic glycolysis, also known as the Warburg effect
BG↓, statistically significant decrease in glucose among participants compliant with fasting compared with controls
Insulin↓, statistically significant decrease in insulin among participants compliant with fasting compared with regular diet before the first cycle of chemotherapy (p = .001), as well as during the middle of therapy
RadioS↑, A complete or partial radiographic response was also noted more often among fasting participants compared with normal diet participants
OS↑, Respondents (n=6,381) aged 50–65 reporting high protein intake had a 75% increase in overall mortality and a 4-fold increase in cancer and diabetes mortality during an 18 year follow up period. (higher OS for low protein)
eff↝, Conversely, in respondents over age 65, high protein intake was associated with reduced cancer and overall mortality.
other↝, Mouse studies confirmed the effect of high protein intake and the GHR-IGF-1 axis on the incidence and progression of breast and melanoma tumors, and also the detrimental effects of a low protein diet in the very old.
OS↑, A sustained state of methionine restriction (MR) dramatically extends the healthspan of several model organisms.
eff↝, we show for the first time that IMR produces similar beneficial metabolic effects to continuous MR,
IGF-1↓, like continuous MR, IMR confers beneficial changes in the plasma levels of the hormones IGF‐1, FGF‐21, leptin, and adiponectin.
adiP↑, Plasma levels of the energy‐regulating hormones adiponectin and leptin are increased and decreased, respectively, by continuous MR
Leptin↓,
Weight↓, both continuous MR and the IMR2 regimen resulted in animals remaining lean over the course of the experiment
Dose↝, Fifteen capsules with pulverized broccoli sprouts containing 90 mg/508 μmol sulforaphane and 180 mg/411 μmol glucoraphanin or methylcellulose were administered daily for up to 1 year.
OS↑, Compared to those of the placebo group, the mean death rate was lower in the treatment group during the first 6 months after intake
eff↝, broccoli sprouts sometimes increased digestive problems, nausea and emesis.
chemoP↑, Studies suggest that fasting before or during chemotherapy may induce differential stress resistance, reducing the adverse effects of chemotherapy and enhancing the efficacy of drugs.
ChemoSen↑,
*DNArepair↑, (1) repairing DNA damage in normal tissues (but not tumor cells);
*Apoptosis↓, preventing apoptosis-mediated damage to normal cells;
*CD8+↑, depleting regulatory T cells and improving the stimulation of CD8 cells;
UPR↑, accumulating unfolded proteins and protecting cancer cells from immune surveillance
eff↝, discuss how ‘fasting-mimicking diet’ as a modified form of fasting enables patients to eat a low calorie, low protein, and low sugar diet while achieving similar metabolic outcomes of fasting.
TumAuto↑, upregulating autophagy flux as a protection against damage to organelles and some cancer cells;
Showing Research Papers: 1 to 50 of 119
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 119
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
Fenton↑, 1, Ferroptosis↑, 1, GPx1↓, 1, GPx1↑, 1, GPx4↓, 2, GSH↓, 3, Iron↑, 1, lipid-P↑, 3, NRF2↓, 2, ROS↑, 19, SOD↓, 2, SOD↑, 1, SOD1↓, 1, SOD1↑, 1, SOD2↓, 1, SOD2↑, 1, TrxR↓, 4,
Metal & Cofactor Biology ⓘ
Ferritin↓, 3, IronCh↑, 1,
Mitochondria & Bioenergetics ⓘ
AIF↑, 2, ATP↓, 3, CDC2↓, 1, ETC↓, 1, Insulin↓, 1, MEK↓, 1, MMP↓, 5, MPT↑, 1, Raf↓, 1, XIAP↓, 1,
Core Metabolism/Glycolysis ⓘ
ACLY↓, 1, adiP↑, 1, AMPK↑, 4, AMPK↝, 1, cMyc↓, 1, ECAR↓, 1, Glycolysis↓, 4, HK2↓, 1, homoC↓, 1, LDH↓, 1, LDH↑, 1, NADPH↓, 1, NADPH↑, 1, PIK3CA↓, 1, p‑S6K↓, 1, SIRT1↑, 1,
Cell Death ⓘ
Akt↓, 8, p‑Akt↓, 1, Apoptosis↑, 9, BAD↑, 1, BAX↑, 4, Bax:Bcl2↑, 3, Bcl-2↓, 3, Casp↑, 1, Casp12↑, 1, Casp3↑, 5, cl‑Casp3↑, 2, Casp8↑, 4, Casp9↑, 4, cl‑Casp9↑, 1, CK2↓, 1, Cyt‑c↑, 4, DR5↑, 2, Fas↑, 3, FasL↑, 2, Ferroptosis↑, 1, JNK↑, 2, MAPK↓, 2, MAPK↑, 1, necrosis↑, 1, p27↑, 2, p38↑, 1, p‑RSK↑, 1, survivin↓, 1, Telomerase↓, 4, TumCD↑, 1,
Kinase & Signal Transduction ⓘ
HER2/EBBR2↓, 1,
Transcription & Epigenetics ⓘ
ac‑H3↓, 1, ac‑H4↓, 1, other↓, 1, other↝, 7,
Protein Folding & ER Stress ⓘ
CHOP↑, 1, ER Stress↑, 1, GRP78/BiP↓, 1, HSP90↓, 1, PERK↑, 1, UPR↑, 1,
Autophagy & Lysosomes ⓘ
BNIP3↝, 1, LC3II↑, 2, p62↓, 2, TumAuto↑, 4,
DNA Damage & Repair ⓘ
DNAdam↑, 7, DNMTs↓, 1, p16↑, 1, P53↑, 1, cl‑PARP↑, 3, PCNA↓, 1,
Cell Cycle & Senescence ⓘ
CDK1↓, 1, CDK2↓, 2, CDK4↓, 4, CDK4↑, 1, CycB/CCNB1↓, 1, cycD1/CCND1↓, 4, CycD3↓, 1, cycE/CCNE↓, 2, P21↑, 1, RB1↑, 1, TumCCA↓, 2, TumCCA↑, 11,
Proliferation, Differentiation & Cell State ⓘ
CD133↓, 1, CSCs↓, 5, Diff↓, 1, EMT↓, 4, ERK↓, 2, ERK↑, 1, FOXO3↑, 1, Gli↓, 1, Gli1↓, 1, HDAC↓, 2, HDAC1↓, 1, HDAC3↓, 1, IGF-1↓, 3, IGF-1↑, 1, mTOR↓, 4, mTOR↝, 1, p‑mTORC1↓, 1, mTORC2↓, 1, n-MYC↓, 1, Nestin↓, 1, NOTCH↓, 2, PI3K↓, 5, PI3K↑, 1, PTEN↑, 1, Smo↓, 1, SOX2↓, 1, STAT3↓, 4, p‑STAT3↓, 1, TOP1↝, 1, TRPM7↓, 1, TumCG↓, 5, Wnt↓, 2, Wnt/(β-catenin)↓, 1,
Migration ⓘ
Ca+2↑, 3, E-cadherin↓, 1, E-cadherin↑, 3, FAK↓, 1, Ki-67↓, 1, MMP2↓, 6, MMP9↓, 6, MMPs↓, 1, PKCδ↓, 1, TET1?, 1, TIMP1↑, 1, TSP-1↑, 1, TumCI↓, 3, TumCMig↓, 4, TumCP↓, 2, TumMeta↓, 1, Twist↓, 1, uPA↓, 3, Vim↓, 1, β-catenin/ZEB1↓, 5,
Angiogenesis & Vasculature ⓘ
angioG↓, 5, angioG↑, 1, EGFR↓, 4, EPR↑, 1, Hif1a↓, 6, VEGF↓, 8, VEGFR2↓, 1,
Barriers & Transport ⓘ
AQPs↓, 1, GLUT1↓, 2,
Immune & Inflammatory Signaling ⓘ
CCR7↓, 1, COX2↓, 5, CXCR4↓, 1, IL1β↓, 1, IL6↓, 3, IL8↓, 2, Inflam↓, 1, JAK2↓, 1, p‑JAK2↓, 1, MCP1↓, 1, NF-kB↓, 4, p‑NF-kB↑, 1, NK cell↑, 2, PGE2↓, 3,
Hormonal & Nuclear Receptors ⓘ
CDK6↓, 1, CDK6↑, 1, Leptin↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 3, BioAv↑, 4, BioAv↝, 2, BioEnh↑, 1, ChemoSen↑, 11, DDS↑, 1, Dose?, 3, Dose↓, 2, Dose↑, 2, Dose↝, 8, Dose∅, 1, eff↓, 2, eff↑, 28, eff↝, 46, Half-Life↓, 1, Half-Life↑, 1, RadioS↑, 6, selectivity↑, 8,
Clinical Biomarkers ⓘ
BG↓, 2, EGFR↓, 4, Ferritin↓, 3, GutMicro↑, 2, HER2/EBBR2↓, 1, IL6↓, 3, Ki-67↓, 1, LDH↓, 1, LDH↑, 1,
Functional Outcomes ⓘ
AntiCan↓, 1, AntiCan↑, 4, AntiTum↑, 1, cardioP↑, 1, chemoP↑, 3, chemoPv↑, 2, ChemoSideEff↓, 1, fatigue↓, 1, hepatoP↑, 1, NDRG1↑, 1, OS↑, 6, OS↝, 1, QoL↑, 1, QoL∅, 1, radioP↑, 1, Risk↓, 4, toxicity↓, 7, toxicity↑, 3, toxicity↝, 1, TumW↓, 1, Weight↓, 1, Weight↑, 2,
Total Targets: 236
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↓, 1, antiOx↑, 3, GPx↑, 1, GSH↑, 2, HDL↑, 1, MDA↓, 1, NRF2↑, 1, OXPHOS↑, 1, ROS↓, 2, SOD↑, 1, VitC↑, 1,
Mitochondria & Bioenergetics ⓘ
MMP↑, 1,
Core Metabolism/Glycolysis ⓘ
adiP↓, 1, LDL↓, 1,
Cell Death ⓘ
Akt↓, 1, Apoptosis↓, 2, Casp3↓, 1, Casp9↓, 1, Cyt‑c↓, 1, MAPK↓, 1,
Kinase & Signal Transduction ⓘ
HCAR2↑, 1,
Transcription & Epigenetics ⓘ
other↑, 3, other↝, 3,
Protein Folding & ER Stress ⓘ
HSP70/HSPA5↑, 1, HSPs↑, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 1, DNArepair↑, 2,
Proliferation, Differentiation & Cell State ⓘ
PI3K↓, 1,
Migration ⓘ
CLDN1↑, 1, MMP9↓, 1, ZO-1↑, 1,
Angiogenesis & Vasculature ⓘ
NO↓, 1,
Immune & Inflammatory Signaling ⓘ
COX1↓, 1, COX2↓, 1, CRP↓, 2, CXCR4↓, 1, HCAR2↑, 1, IL17↓, 1, IL18↓, 1, IL1β↓, 2, IL6↓, 1, Imm↑, 2, Inflam↓, 6, PGE2↓, 1, TNF-α↓, 1,
Synaptic & Neurotransmission ⓘ
AChE∅, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 2, BioAv↑, 1, Dose↑, 1, Dose⇅, 1, eff↓, 5, eff↑, 1, eff↝, 6, Half-Life↑, 1, Half-Life↝, 1,
Clinical Biomarkers ⓘ
BP↓, 1, CRP↓, 2, GutMicro↑, 2, IL6↓, 1,
Functional Outcomes ⓘ
BOLD↑, 1, cachexia↓, 1, cardioP↑, 3, cognitive↑, 2, hepatoP↑, 1, memory↑, 2, Mood↑, 1, neuroP↑, 4, Risk↓, 4, toxicity↓, 3, toxicity↝, 2, toxicity∅, 1, Weight↓, 1, Wound Healing↑, 1,
Infection & Microbiome ⓘ
CD8+↑, 1,
Total Targets: 74
Scientific Paper Hit Count for: eff, efficacy
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include :
-low or high Dose
-format for product, such as nano of lipid formations
-different cell line effects
-synergies with other products
-if effect was for normal or cancerous cells
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