AntiCan Cancer Research Results
AntiCan, Anticancer Effect: Click to Expand ⟱
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Anticancer Effect
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Scientific Papers found: Click to Expand⟱
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.
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AD, |
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Stroke, |
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AntiCan↓, anticancer, antidiabetic, antimicrobial, antiaging, neuroprotective, cardioprotective, respiratory protective, gastroprotective, hepatic protective, and renal protective effects
*neuroP↑,
*cardioP↑, Cardioprotective action of baicalein
*hepatoP↑,
*RenoP↑, baicalein’s capacity to lessen cisplatin-induced nephrotoxicity is probably due, at least in part, to the attenuation of renal oxidative and/or nitrative stress
TumCCA↑, Baicalein induces G1/S arrest in lung squamous carcinoma (CH27) cells by downregulating CDK4 and cyclin D1, as well as upregulating cyclin E
CDK4↓,
cycD1/CCND1↓,
cycE/CCNE↑,
BAX↑, SGC-7901 cells showed that when baicalein was administered, Bcl-2 was downregulated and Bax was increased
Bcl-2↓,
VEGF↓, Baicalein inhibits the synthesis of vascular endothelial growth factor (VEGF), HIF-1, c-Myc, and nuclear factor kappa B (NF-κB) in the G1 and S phases of ovarian cancer cell
Hif1a↓,
cMyc↓,
NF-kB↓,
ROS↑, Baicalein produced intracellular reactive oxygen species (ROS) and activated BNIP3 to slow down the development and hasten the apoptosis of MG-63,OS cell
BNIP3↑,
*neuroP↑, Baicalein exhibits neuroprotective qualities against amyloid (AN) functions by preventing AN from aggregating in PC12 neuronal cells to cause A𝛽-induced cytotoxicity
*cognitive↑, baicalein encourages non-amyloidogenic processing of APP, which lowers the generation of A𝛽 and enhances cognitive function
*NO↓, baicalein effectively reduced NO generation and iNOS gene expression
*iNOS↓,
*COX2↓, Baicalein therapy significantly decreased the expression of COX-2 and iNOS, as well as PGE2 and NF-κB, indicating a protective effect against cerebral I/R injury.
*PGE2↓,
*NRF2↑, Baicalein therapy markedly elevated nuclear Nrf2 expression and AMPK phosphorylation in the ischemic cerebral cortex
*p‑AMPK↑,
*Ferroptosis↓, Baicalein suppressed ferroptosis associated with 12/15-LOX, hence lessening the severity of post-traumatic epileptic episodes generated by FeCl3
*lipid-P↓, HT22 cells were damaged by ferroptosis, which is mitigated by baicalein may be due to its lipid peroxidation inhibitor
*ALAT↓, Baicalin lowers the raised levels of hepatic markers alanine transaminase (ALT), aspartate aminotransferase (AST)
*AST↓,
*Fas↓, Baicalin has also been shown to suppress apoptosis, decrease FAS protein expression, block the caspase-8 pathway, and decrease Bax protein production
*BAX↓,
*Apoptosis↓,
*AntiCan↓, Baicalein is known to display anticancer activity through the inhibition of inflammation and cell proliferation
*Inflam↓,
TumCP↓,
NF-kB↓, baicalein decreased the activation of nuclear factor-κB (NF-κB)
PPARγ↑, anti-inflammatory effects of baicalein might be initiated via PPARγ activation.
TumCCA↑, baicalein inhibited cell cycle progression and cell growth, and promoted apoptosis of cancer cells
JAK2↓, inactivation of the signaling pathway JAK2/STAT3 [63]
STAT3↓,
TumCMig↓, baicalein suppressed migration as well as invasion through decreasing the aerobic glycolysis and expression of MMP-2/9 proteins.
Glycolysis↓,
MMP2↓,
MMP9↓,
selectivity↑, Furthermore, baicalein and baicalin had less inhibitory effects on normal ovarian cells’ viability.
VEGF↓, baicalein is more effective in inhibiting the expressions of VEGF, HIF-1α, cMyc, and NFκB
Hif1a↓,
cMyc↓,
ChemoSen↑, baicalein enhanced the cisplatin sensitivity of SGC-7901/DDP gastric cancer cells by inducing autophagy and apoptosis through the Akt/mTOR and Keap 1/Nrf2 pathways
ROS↑, oral squamous cell carcinoma Cal27 cells. Significantly, it was noticed that baicalein activated reactive oxygen species (ROS) generation in Cal27 cells
p‑mTOR↓, results suggest that p-mTOR, p-Akt, p-IκB, and NF-κB protein expressions were decreased
PTEN↑, Baicalein upregulated PTEN expression, downregulated miR-424-3p, and downregulated PI3K and p-Akt.
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Arthritis, |
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*AntiCan↑, Emerging studies show that it displays potent anti-tumor activity in several human cancers.
*TRPV1↑, The “heat-sensation” of capsaicin arises due to the binding of capsaicin to transient receptor potential vanilloid (TRPV) ion-channel receptors
*cardioP↑, some of the biological activities of capsaicin, like its anti-neoplastic, cardioprotective effects, have been found to be independent of the TRPV1 receptor.
AntiCan↓, Exposure to high doses of capsaicin (above 100 mg capsaicin per kg body weight) for a prolonged time causes peptic ulcers, accelerates the development of prostate, stomach, duodenal, and liver cancers and enhances breast cancer metastasis [5, 6].
Apoptosis↑, Capsaicin induces robust apoptosis in multiple types of human cancer cells both in vitro and in mice models.
ChemoSen↑, Capsaicin potentiates the apoptotic activity of cisplatin in human stomach cancer and attenuates cisplatin-induced renal toxicity in rodent models
*Inflam↓, oral or local administration of capsaicin reduces inflammation and pain from rheumatoid arthritis, fibromyalgia and chemical hyperalgesia
*Pain↓,
*AntiAg↑, The anti-platelet and anti-coagulant activity of capsaicin was independent of TRPV1
*Weight↓, capsaicinoids show anti-obesity activity by enhancing energy expenditure of the body
*BioAv↑, Capsaicin is robustly absorbed from the skin upon topical administration [4]
BioAv↑, capsaicin is rapidly absorbed from the stomach and the intestine following oral administration.
Half-Life↝, The liver and kidney displayed maximal amounts of capsaicin in 3 hours and 6 hours, respectively.
Half-Life↓, An interesting fact to note is that the bioavailability and half-life of capsaicin is quite low in the plasma, irrespective of the route of administration.
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vitro+vivo, |
Bladder, |
5637 |
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in-vitro, |
Bladder, |
T24/HTB-9 |
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antiOx↑, Capsaicin (CAP), a highly selective agonist for transient receptor potential vanilloid type 1 (TRPV1), has been widely reported to exhibit anti-oxidant, anti-inflammation and anticancer activities.
Inflam↓,
AntiCan↓,
TRPV1↑, CAP could specifically activate TRPV1 [12,13] and interfere with the calcium signaling pathway
TumCP↓, CAP could suppress BCa tumorigenesis by inhibiting its proliferation both in vitro and in vivo.
TumCCA↑, CAP induced cell cycle arrest at G0/G1 phase and ROS production.
ROS↑,
FOXO3↑, strong increase of FOXO3a after treatment with CAP.
TumCMig↓, CAP Inhibited BCa Cell Proliferation and Migration
AntiCan↓, Capsaicin, which is the pungent ingredient of red hot chili peppers, has been reported to possess anticancer activity, including that against hepatocellular carcinoma.
Apoptosis↑, Capsaicin can induce apoptosis in HepG2 cells.
cl‑PARP↑, The expression levels of CL-PARP and Bcl-2 were significantly increased.
Bcl-2↑,
TumAuto↑, capsaicin can trigger autophagy in HepG2 cells.
LC3II↑, Capsaicin increased LC3-II and beclin-1 expression and GFP-LC3-positive autophagosomes.
eff↑, Pharmacological or genetic inhibition of autophagy further sensitized HepG2 cells to capsaicin-induced apoptosis.
STAT3↑, capsaicin upregulated the Stat3 activity which contributed to autophagy
ROS↑, capsaicin triggered reactive oxygen species (ROS) generation in hepatoma cells
eff↓, and that the levels of ROS decreased with N-acetyl-cysteine (NAC), a ROS scavenger.
*AntiCan↓, Coenzyme Q10 (CoQ10) is a naturally occurring component that performs an anticancer function by reducing oxidative stress.
*ROS↓,
chemoPv↑, As a defensive mechanism against oxidative stress elevation in the antioxidative level including CoQ10 is expected, and an increase in these agents can protect cells and organs from side effects of chemotherapeutic drugs.
TumCCA↑, CoQ10 may induce its antitumor effect through multiple mechanisms, including anti-oxidation, anti-inflammation, cell cycle arrest, promoting apoptosis, reducing cell proliferation, inhibiting angiogenesis, suppression of MMPs, and so on
Apoptosis↑,
TumCP↓,
angioG↓,
MMPs↓,
ChemoSen∅, The review points out that: Some studies show improved tolerance without reduced response (chatAI interpretation)
Inflam↓, known or suspected (anti-inflammatory, antivirus, antiulcer, anticarcinogenesis, and others
AntiCan↓,
DNAdam↓, Licorice and its derivatives may protect against carcinogen-induced DNA damage
LOX1↓, Glycyrrhizic acid is an inhibitor of lipoxygenase and cyclooxygenase, inhibits protein kinase C, and downregulates the epidermal growth factor receptor
COX2↓,
PKCδ↓,
EGFR↓,
eff↑, Bicarbonate markedly enhances the anticancer activity of TACE.
Dose↝, The patients were treated with transarterial chemoembolization (TACE) with or without bicarbonate local infusion into tumor.
other↓, geometric mean of viable tumor residues (VTR) in TACE with bicarbonate was 6.4-fold lower than that in TACE without bicarbonate
OS↑, The survival data suggested that bicarbonate may bring survival benefit.
toxicity↓, It was within our expectation, as locally administration of bicarbonate into tumor is safe.
AntiCan↓, Taken together, this pilot study demonstrated that bicarbonate infusion locally into HCC can markedly enhance anticancer activity of TACE,
AntiCan↓, Naringenin exhibits lipid-lowering and insulin-like characteristics and is used to treat osteoporosis, cancer and cardiovascular disorders
CYP19↓, controlling breast and prostate cancer by inhibition of CYP19
PI3K↓, naringin suppresses the PI3K/AKT signalling pathway
Akt↓,
TumAuto↑, triggers autophagy
eff↑, Naringin and naringenin co-administration or pre-administration has enhanced the target drug’s potency and produced a synergistic effect
BioEnh↑, potential applications of Naringin and Naringenin as recognized bio-enhancers.
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vitro+vivo, |
Lung, |
H1299 |
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H226 |
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AntiCan↓, Isothiocyanates (ITCs) are natural compounds and inhibit the tumorigenesis of various cancers.
TumCP↓, Our previous studies show that ITCs inhibit the proliferation and metastasis of non-small cell lung cancer (NSCLC) cells, and have synergistic effects with chemotherapy drugs
TumMeta↓,
ChemoSen↑,
tumCV↓, We showed that phenethyl isothiocyanate (PEITC) dose-dependently inhibited the cell viability of both NSCLC cell lines H1299 and H226 with IC50 values of 17.6 and 15.2 μM, respectively.
TumCI↓, Furthermore, PEITC dose-dependently inhibited the invasion and migration of H1299 and H226 cells.
TumCMig↓,
FTO↓, PEITC treatment dose-dependently increased m6A methylation levels and inhibited the expression of the m6A demethylase fat mass and obesity-associated protein (FTO) in H1299 and H226 cells
TLE1↓, Moreover, we showed that PEITC suppressed the migration of NSCLC cells by inhibiting TLE1 expression and downstream Akt/NF-κB pathway.
Akt↓,
NF-kB↓,
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BioAv↝, Urolithin A (UA), a metabolite derived from ellagic acid through gut microbiota metabolism, has emerged as a compelling anticancer agent.
TumAuto↝, UA has multiple mechanisms of action, including the regulation of autophagy, enhancement of mitochondrial function, and inhibition of tumor progression and metastatic pathways.
TumCG↓,
TumMeta↓,
ChemoSen↑, Additionally, its chemo-, immuno-, and radio-sensitization properties further increase its therapeutic advantages
Imm↑,
RadioS↑,
BioAv↑, Nanotechnology-driven approaches, such as nanoparticle formulations, lipids, and powder formulations, have successfully increased the solubility, stability, bioavailability, precise targeted delivery to cancer tissues
other↝, While sparingly soluble in water, UA shows better solubility in organic solvents, such as ethanol and dimethyl sulfoxide.
eff↓, prone to degradation at extreme pH values or high temperatures.
*antiOx↓, UA has gained increasing attention for its pharmacological properties, including anti-oxidant, anti-inflammatory, and anti-cancer activities.
*Inflam↓,
AntiCan↓,
AntiAge↑, UA has potential as a key component in antiaging interventions.
chemoP↑, UA can counteract age-related muscle wasting and enhance physical performance, making it a valuable therapeutic for improving muscle health and combating sarcopenia
*neuroP↑, UA has neuroprotective properties because of its ability to reduce neuroinflammation, improve mitochondrial function, and mitigate oxidative stress,
*ROS↓,
*cognitive↑, suggesting its potential application in neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, and other age-related cognitive disorders)
*lipid-P↓, UA to reduce lipid peroxidation, combat oxidative stress, and improve endothelial function, promoting its role in cardiovascular health
*cardioP↑,
*TNF-α↓, exerts anti-inflammatory effects by suppressing the production of proinflammatory cytokines, such as TNF-α and IL-6, which can be employed for the management of chronic inflammatory conditions (such as rheumatoid arthritis and inflammatory bowel dise
*IL6↓,
GutMicro↑, Given that UA formation and bioactivity are influenced by the gut microbiota, its supplementation could promote a healthier gut microbiome, with potential therapeutic benefits for a wide range of conditions, including irritable bowel syndrome.
TumCCA↑, UA has potent anticancer effects through cell cycle arrest, apoptosis induction, and the modulation of oncogenic signaling pathways.
Apoptosis↑,
angioG↓, regulate the tumor microenvironment by inhibiting angiogenesis and inflammation
NF-kB↓, UA inhibited key signaling pathways, such as the NF-κB and PI3K/AKT pathways, which are critical for tumor progression
PI3K↓,
Akt↓,
Casp↑, UA also promoted apoptosis via the activation of caspases and the downregulation of survival proteins such as Survivin
survivin↓,
TumCP↓, inhibited MCF-7 cell proliferation in vitro and significantly reduced 27-HC-induced tumor growth in vivo.
cycD1/CCND1↓, UA induced cell cycle arrest by downregulating cyclin D1 and c-MYC and promoted apoptosis by increasing the expression of proapoptotic proteins such as Bax while reducing antiapoptotic BCL2 levels.
cMyc↑,
BAX↑,
Bcl-2↓,
COX2↓, UA, a metabolite of pomegranate mesocarp, synergistically reduced COX-2 expression by ~70% and increased cleaved caspase-3 levels
P53↑, UA induces the expression of tumor suppressor proteins such as p53 and p38-MAPK
p38↑,
*ROS↓, UA demonstrates significant antioxidant activity by reducing reactive oxygen species levels and enhancing the activities of key antioxidant enzymes, such as superoxide dismutase and glutathione peroxidase.
*SOD↑,
*GPx↑,
SIRT1↑, UA induced cell cycle arrest and apoptosis while enhancing the expression of key tumor suppressors, including Sirtuin 1 (Sirt1) and Forkhead box protein O1 (FOXO1)
FOXO1↑,
eff↑, UA preferentially accumulates in prostate and intestinal tissues, suggesting its targeted bioactivity.
ChemoSen↑, UA has emerged as a potent chemosensitizing agent that enhances the efficacy of conventional cancer therapies.
Showing Research Papers: 1 to 12 of 12
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, GPx4↓, 1, ROS↑, 4, TrxR↓, 1,
Core Metabolism/Glycolysis ⓘ
cMyc↓, 2, cMyc↑, 1, Glycolysis↓, 1, PPARγ↑, 1, SIRT1↑, 1,
Cell Death ⓘ
Akt↓, 3, Apoptosis↑, 4, BAX↑, 2, Bcl-2↓, 2, Bcl-2↑, 1, Casp↑, 1, p38↑, 1, survivin↓, 1, TRPV1↑, 1,
Transcription & Epigenetics ⓘ
other↓, 1, other↝, 1, TLE1↓, 1, tumCV↓, 1,
Autophagy & Lysosomes ⓘ
BNIP3↑, 1, LC3II↑, 1, TumAuto↑, 2, TumAuto↝, 1,
DNA Damage & Repair ⓘ
DNAdam↓, 1, DNAdam↑, 1, P53↑, 1, cl‑PARP↑, 1,
Cell Cycle & Senescence ⓘ
CDK4↓, 1, cycD1/CCND1↓, 2, cycE/CCNE↑, 1, TumCCA↑, 5,
Proliferation, Differentiation & Cell State ⓘ
FOXO1↑, 1, FOXO3↑, 1, p‑mTOR↓, 1, PI3K↓, 2, PTEN↑, 1, STAT3↓, 1, STAT3↑, 1, TumCG↓, 1,
Migration ⓘ
FTO↓, 1, MMP2↓, 1, MMP9↓, 1, MMPs↓, 1, PKCδ↓, 1, TumCI↓, 1, TumCMig↓, 3, TumCP↓, 5, TumMeta↓, 2,
Angiogenesis & Vasculature ⓘ
angioG↓, 2, EGFR↓, 1, Hif1a↓, 2, LOX1↓, 1, VEGF↓, 2,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, Imm↑, 1, Inflam↓, 2, JAK2↓, 1, NF-kB↓, 4,
Hormonal & Nuclear Receptors ⓘ
CYP19↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↑, 2, BioAv↝, 1, BioEnh↑, 1, ChemoSen↑, 5, ChemoSen∅, 1, Dose↝, 1, eff↓, 2, eff↑, 4, eff↝, 1, Half-Life↓, 1, Half-Life↝, 1, RadioS↑, 1, selectivity↑, 1,
Clinical Biomarkers ⓘ
EGFR↓, 1, GutMicro↑, 1,
Functional Outcomes ⓘ
AntiAge↑, 1, AntiCan↓, 10, chemoP↑, 1, chemoPv↑, 1, OS↑, 1, toxicity↓, 2,
Total Targets: 83
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↓, 1, Ferroptosis↓, 1, GPx↑, 1, lipid-P↓, 2, NRF2↑, 1, ROS↓, 3, SOD↑, 1,
Core Metabolism/Glycolysis ⓘ
ALAT↓, 1, p‑AMPK↑, 1,
Cell Death ⓘ
Apoptosis↓, 1, BAX↓, 1, Fas↓, 1, Ferroptosis↓, 1, iNOS↓, 1, TRPV1↑, 1,
Migration ⓘ
AntiAg↑, 1,
Angiogenesis & Vasculature ⓘ
NO↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IL6↓, 1, Inflam↓, 3, PGE2↓, 1, TNF-α↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↑, 1,
Clinical Biomarkers ⓘ
ALAT↓, 1, AST↓, 1, IL6↓, 1,
Functional Outcomes ⓘ
AntiCan↓, 2, AntiCan↑, 1, cardioP↑, 3, cognitive↑, 2, hepatoP↑, 1, neuroP↑, 3, Pain↓, 1, RenoP↑, 1, Weight↓, 1,
Total Targets: 35
Scientific Paper Hit Count for: AntiCan, Anticancer Effect
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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