Dose Cancer Research Results
Dose, Dosage: Click to Expand ⟱
| Source: |
| Type: |
Drug dosage vs efficacy, and actual dosage number of research papers.
|
Scientific Papers found: Click to Expand⟱
*Dose?, Subjects received orally 6 mg (p.o.) of auranofin daily, the recommended dose for rheumatoid arthritis, for 7 days and were followed for 126 days.
*Half-Life↝, The mean gold maximum concentration in plasma (Cmax) at day 7 was 0.312 μg/ml and the half-life (t1/2) 35 days, so steady-state blood levels would not be reached in short-term therapy.
*Dose↑, The highest concentration of gold, 13 μM (auranofin equivalent), or more than 25× the 50% inhibitory concentration (IC50) for E. histolytica and 4× that for Giardia, was in feces at 7 days.
*toxicity↝, Long-term (months to years) auranofin therapy was linked to side effects, including diarrhea (40% of subjects), skin rashes (2% to 5%), hematologic abnormalities (rare), and proteinuria (5%)
*Bacteria↓, Higher doses of auranofin will clearly be required for some infections.
*Dose↑, The FDA has approved clinical trials using auranofin at up to 21 mg/day for treatment of relapsed chronic lymphocytic leukemia after daily doses of 9 and 12 mg for at least 28 days were well tolerated
Dose?, glucose concentration was examined by varying the concentration of glucose from 0.001 to 0.01 M in 0.1 M NaOH at the scan rate of 50 mV/s. The charges increased with increasing the glucose concentration up to 7 mM, and then leveled off
Dose?, Apigenin in parsley, dried: 4503.50mg/100g(AVG), 1774.60mg/100g(MIN), 13506.22mg/100g(MAX),
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.
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 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↑,
*ROS↑, beta-carotene is known to have pro-oxidant activity in vitro
*ROS⇅, The present study in Hs68 cells demonstrates that lycopene can be either an antioxidant or a pro-oxidant depending on the oxidants used, and that lycopene and beta-carotene behave similarly under the in vitro oxidative conditions.
*Dose?, Both the antioxidant and pro-oxidant effects of lycopene tended to be dose-dependent
*Inflam↓, brusatol exhibits remarkable anti-inflammatory efficacy in murine models with ulcerative colitis, significantly diminishing serum levels of pro-inflammatory cytokines (e.g., IL-17 and TNF-α), inhibiting IL-22/STAT3 pathway activation,
*IL17↓,
*TNF-α↓,
*IL22↓,
*STAT3↓,
*other↝, brusatol holds promising therapeutic potential in regulating psoriasis with dyslipidemia.
*eff↑, Brusatol significantly reverses the protein profile in IMQ-induced psoriasiform skin lesions
*Dose?, treatment group (Bru) administered brusatol (9.2 mg/kg) via oral gavage for seven consecutive days.
ROS↑, CA can become a pro-oxidant due to its ability to chelate metals such as copper (Cu)
antiOx↑, CA, including its antioxidant, anti-inflammatory, and anticancer properties.
Inflam↓,
AntiCan↑,
NF-kB↓, ability to modulate several pathways, such as inhibiting NFkB, STAT3, and ERK1/2
STAT3↓,
ERK↓,
ChemoSen↑, mitigation of chemotherapy and radiotherapy-induced toxicity
RadioS↑,
AMPK↑, CA (100 μM) alone or in combination with metformin (10 mM) is efficient in stimulating the AMPK signaling pathway, which acts by preventing de novo synthesis of unsaturated fatty acids, consequently reducing cancer cell survival
eff↑, combined treatment with cisplatin (5 µM) and CA (10 µM) restored the chemo-sensitizing effect against cisplatin-resistant ovarian endometrioid adenocarcinoma cells (A2780)
selectivity↑, dual capacity of CA to act as an antioxidant during carcinogenesis and as a pro-oxidant against cancer cells, promoting their apoptosis or sensitizing them to chemotherapeutic drugs
COX2↓, CA has been discovered to impede Cyclooxygenase-2 (COX-2), an enzyme pivotal in the inflammatory cascade.
Dose∅, 50 to 10 µM, effectively suppresses COX-2
PHDs↓, CA serves as a potent inhibitor of prolyl hydroxylase-2 (PHD2),
MMP9↓, CA has been identified as an inhibitor of MMP-9
MMP2↓, CA and CAPE at doses of 5 mg/kg subcutaneously or 20 mg/kg orally. Both compounds exhibited the inhibition of MMP-2 and -9,
Dose∅, CA (0–200 μM) induces apoptosis and cell cycle arrest by increasing the expression profile of caspase 1 and caspase 3
Dose∅, CA (200–800 μM) has been shown to promote Ca2+ accumulation
Ca+2↑,
Dose?, Treatment with CA at a concentration of 20 μM disrupts mitochondrial function, which leads to several effects: increased Caspase-9 activity, elevated levels of ROS, and a decrease in membrane potential (Δψm)
MMP↓,
RadioS↑, Studies conducted on cells and animals indicate that CA enhances the efficacy of chemotherapy and radiotherapy, potentially mitigating their adverse effects and improving patient outcomes with minimal side effects
ENOX2↑, low concentrations s (<10uM) of capsaicin up-regulates tNOX
TumCP↑,
TumCMig↑,
Dose?, <10uM
eff↑, tNOX knockdown reverses capsaicin-induced cell migration and growth
Dose?, At low concentration, citrate increased both histone H4 acetylation and lipid deposition; at high concentration, citrate inhibited both
ac‑H4↓,
lipidDe↓,
ACLY↓, Considering the strong demand for acetyl-CoA but not for OAA in tumor cells, the exogenous citrate would behave like a trojan horse that carries OAA inside the cells and reduces ACLY expression and cellular metabolism.
selectivity↑, in non-tumor cells, changes of acetylated histone level do not correspond to a change of ACLY expression, as instead shown by HepG2 cells.
*ACLY∅, In contrast, ACLY expression in IHH (normal)cells was not modified after citrate exposure, suggesting that, in this case, ACLY expression was not regulated by histone H4 acetylation
Glycolysis↓, strong inhibition of glycolysis, which leads to a decrease in NADH necessary for OAA reduction
NADH↓,
OAA↑, exogenous citrate would behave like a trojan horse that releases OAA in the cells, where it could exert its therapeutic effect also on hepatoma cells.
other↑, most important discovery is undoubtedly the demonstration that high concentrations of citrate decrease the availability of acetyl-CoA, a key molecule both in the metabolism of sugars and lipids
TCA↑,
FASN↑, Cytosolic acetyl-CoA sustains fatty acid (FA) synthesis (FAS)
Glycolysis↓,
glucoNG↑, while it enhances gluconeogenesis by promoting fructose-1,6-biphosphatase (FBPase)
PFK1↓, citrate directly inhibits the main regulators of glycolysis, phosphofructokinase-1 (PFK1) and phosphofructokinase-2 (PFK2)
PFK2↓, well-known inhibitor of PFK
FBPase↑, enhances gluconeogenesis by promoting fructose-1,6-biphosphatase (FBPase)
TumCP↓, inhibits the proliferation of various cancer cells of solid tumors (human mesothelioma, gastric and ovarian cancer cells) at high concentrations (10–20 mM),
eff↑, promoting apoptosis and the sensitization of cells to cisplatin
ACLY↓, higher concentrations (10 mM or more) decreased both acetylation and ACLY expression
Dose↑, In various cell lines, a high concentration of citrate—generally above 10 mM—inhibits the proliferation of cancer cells in a dose dependent manner
Casp3↑,
Casp2↑,
Casp8↑,
Casp9↑,
Bcl-xL↓,
Mcl-1↓,
IGF-1R↓, citrate at high concentration (10 mM) also inhibits the insulin-like growth factor-1 receptor (IGF-1R)
PI3K↓, pathways
Akt↓, activates PTEN, the key phosphatase inhibiting the PI3K/Akt pathway
mTOR↓,
PTEN↑, high dose of citrate activates PTEN
ChemoSen↑, citrate increases the sensibility of cells to chemotherapy (in particular, cisplatin)
Dose?, oral gavage of citrate sodium (4 g/kg twice a day) for several weeks (4 to 7 weeks) significantly regressed tumors
Risk↓, CoQ10, an essential compound for cellular energy production, is often found at low levels in cancer patients, suggesting a link between CoQ10 deficiency and cancer risk
TumCG↓, Research shows CoQ10 helps fight cancer by slowing tumor growth, preventing new blood vessel formation in tumors and triggering self-destruction of abnormal cells
angioG↓,
TumCD↑,
*toxicity↓, The compound helps regulate immune function and inflammation by supporting
mitochondrial health and enhancing T-cell activity, while showing minimal side effects
even at high doses
*BioAv↑, Simple steps, like splitting doses and pairing CoQ10 with a meal containing fats, aid in its
absorption and effectiveness
MMPs↓, reported ability of CoQ10 to suppress something known
as MMPs (matrix metalloproteinases)
Inflam↓, A further aspect focused on the anti-inflammatory effects of CoQ10
chemoP↑, Some individuals received
significant help in diminishing tumor markers, while others used CoQ10 to mitigate drug
side effects.
cardioP↑, According to the authors, coenzyme Q10 shows evidence
of lowering that heart strain.
*ROS↓, Researchers explained that coenzyme Q10 is a compound naturally made in your body,
essential for mitochondrial energy production and normal oxidative processes
*toxicity↝, Liver enzyme elevation has been reported after prolonged use of doses of
300 milligrams (mg) daily, but this effect did not escalate into overt liver damage.
Dose?, If you have never taken CoQ10 before, aim for 200 mg to 300 mg daily for the first three weeks. After about 21 days, step down to 100 mg daily
TOP1↓, Top1 is the selective target of camptothecins, which are effective anticancer agents.
AntiCan↑,
Dose?, Two camptothecin derivatives are used in cancer therapy: hycamtin (Topotecan®) and CPT-11 (Irinotecan; Camptosar®) [31].
CHK1↑, Chk1 activation by camptothecin
Chk2↑, Chk2 activation by camptothecin
*CRM↓, AcCoA depleting agents (e.g., hydroxycitrate),
*Dose?, acetyltransferase inhibitors (e.g., anacardic acid, curcumin, epigallocatechin-3-gallate, garcinol, spermidine)
*AntiAge↑, Another common characteristic of these agents is their capacity to reduce aging-associated diseases and to confer protective responses against ischemia-induced organ damage.
*Acetyl-CoA↓, Altogether, these observations point to the idea that starvation causes autophagy because it results in the early depletion of AcCoA
*SIRT1↑, nduction of the deacetylase activity of sirtuins (as a result of changing NADH/NAD+ ratios and increased SIRT1 expression)
*AMPK↑, activation of AMPK activity (as a result of changing ATP/ADP ratios)
*mTORC1↓, inhibition of MTORC1 (as a result of amino acid depletion).
*AntiAge↑, CR or intermittent fasting are known for their wide life-span-extending
chemoP↑, fasting can reduce the subjective and objective toxicity of cytotoxic anticancer chemotherapies, both in humans and in mouse models, at the same time that it improves treatment outcome in mice
*MAOA↓, MAO activity was inhibited by curcumin and ellagic acid
*Dose∅, however, higher half maximal inhibitory concentrations of curcumin (500.46 nM) and ellagic acid (412.24 nM)
Dose?, MAO-B by curcumin (IC50 500.46 nM) and ellagic acid (IC50 412.24 nM)
| - |
in-vitro, |
Cerv, |
HeLa |
|
|
|
- |
in-vitro, |
Nor, |
MCF10 |
|
|
|
selectivity↑, EGCg preferentially inhibited growth of HeLa and mammary adenocarcinoma cells compared with growth of mammary epithelial cells
*toxicity∅, Mammary epithelial cells recovered from EGCg treatment even at 50 mM
TumCG↓, growth of HeLa and mammary adenocarcinoma cells was inhibited by EGCg at concentrations as low as 1 mM.
With repeated additions of 100 nM EGCg (every 2 hr during the day), growth was inhibited during the day but recovered during the night
NADHdeh?,
eff↑, Green tea infusions
were approximately 10 times more effective than those of
black tea and contained approximately 10 times more
EGCg
ENOX2↓, EGCg inhibit the NADH oxidase(ENOX2) of plasma membrane vesicles from cancer cells and not that of normal cells,
Dose?, with repeated additions (twice daily) at 1 mM EGCg, the EGCg concentration achieving complete inhibition of tNOX in BT-20 cells, growth inhibition and apoptosis in BT-20 cells were achieved.
Risk↓, Increasing physical activity is associated with meaningful reductions in the risk of breast cancer,
Dose?, Compared to the lowest level of physical activity, the highest level was associated with a summary relative risk (SRR) of 0.88 for all breast cancer, 0.89 for ER+/PR+ breast cancer and 0.8 for ER-/PR- breast cancer.
eff↑, Findings indicate that a physically inactive women engaging in at least 150 min per week of vigorous physical activity would reduce their lifetime risk of breast cancer by 9%
Dose?, mean inhibitory concentration (IC50 ) ... fenbendazole were 0.550 ± 0.015, 1.530 ± 0.159 and 0.690 ± 0.095 μM
selectivity↑, treatment of primary canine fibroblasts for 72 h at IC50 showed no significant effect.
TumCD↑, Mebendazole and fenbendazole are cytotoxic in canine glioma cell lines in vitro and may be good candidates for treatment of canine gliomas.
α-tubulin↓, Immunofluorescence studies showed disruption of tubulin after treatment
| - |
in-vitro, |
HCC, |
SMMC-7721 cell |
|
|
|
AntiTum↑, Gambogic acid (GA), a natural product that has been used in traditional Chinese medicine for centuries, demonstrates potent anticancer activity in numerous types of human cancer cells and has entered phase II clinical trials
TrxR↓, GA may interact with TrxR1 to elicit oxidative stress
TrxR1↓,
ROS↑,
Apoptosis↑, eventually induce apoptosis in human hepatocellular carcinoma SMMC-7721 cells.
Dose∅, GA effectively inhibited TrxR1 with an IC 50 around 1.2 uM,
Dose?, Under our experimental conditions, GA with concentration less than 5 uM gives only marginal inhibition
of Trx
NF-kB↓,
TRAILR↑, Artepillin C increased the expression of TRAIL-R2 and decreased the activity of NF-κB
Casp8↑, Co-treatment with TRAIL and artepillin C induced the significant activation of caspase-8 and caspase-3, as well as the disruption of ΔΨm
Casp3↑,
MMP↓,
Dose?, co-treatment of LNCaP cells with 100 ng/ml TRAIL and 50–100 μM artepillin C for 24 h the cytotoxicity ranged from 59.3±1.6 to 66.3±2.3%.
| - |
in-vitro, |
Nor, |
MCF10 |
|
|
|
- |
in-vitro, |
BC, |
MDA-MB-231 |
|
|
|
- |
in-vitro, |
BC, |
MDA-MB-468 |
|
|
|
- |
in-vitro, |
PC, |
Bxpc-3 |
|
|
|
TumCP↓,
Apoptosis↑,
eff↓, cell death is prevented to a significant extent by cuprous chelator neocuproine and reactive oxygen species scavengers
*toxicity↑, normal breast epithelial cells, cultured in a medium supplemented with copper, become sensitized to polyphenol-induced growth inhibition.
Dose?, apigenin at 5uM promoted growth in MCF10A cells and PC3 cancer cells. This could be because polyphenols at lower concentrations are known to be associated with
cell proliferation [21], while behaving as prooxidants at high concentrations
eff↓, Apigenin- and luteolin-induced antiproliferation and apoptosis in cancer cells is inhibited by cuprous chelator but not by iron and zinc chelators
eff↓, EGCG and resveratrol, similar to that of the flavones luteolin and apigenin, also involves the mobilization of endogenous copper and consequent prooxidant effect leading to cell death.
Dose?, Caffeic acid (0.639–4.172 mg/g propolis) and galangin (1.317–8.551 mg/g propolis) were found to be the predominant phenolic compounds in these propolis extracts.
antiOx↑, Propolis from West Macedonia showed higher antioxidant activities than propolis from Rhodes.
other↑, West Macedonia propolis presented the highest amount of total phenolic compounds, especially phenolic acids and flavonoids.
MMPs↓, inhibition of matrix metalloproteinases, anti-angiogenesis
angioG↓,
TumMeta↓, prevention of metastasis, cell-cycle arrest
TumCCA↑,
Apoptosis↑,
ChemoSideEff↓, moderation of the chemotherapy-induced deleterious side effects
eff∅, components conferring antitumor potentials have been identified as caffeic acid phenethyl ester, chrysin, artepillin C, nemorosone, galangin, cardanol, etc
HDAC↓, Taiwanese green propolis extract was used to develop an anticancer agent
NBM-HD-3, a histone deacetylase inhibitor (HDACis).
PTEN↑, found to increase phosphatase and tensin homolog (PTEN) and protein kinase B (Akt) protein levelssignificantly, while decreasing phospho-PTEN and phospho-Akt levels markedly
p‑PTEN↓,
p‑Akt↓,
Casp3↑, Propolis induced apoptosis and caspase 3 cleavage, increased phosphorylation of extracellular signal regulated kinase 1/2 (ERK1/2), protein kinase B/Akt1 and focal adhesion kinase (FAK).
p‑ERK↑,
p‑FAK↑,
Dose?, When administered orally for 20 weeks at a dose of 100-300 mg/kg, the protective role against the lingual carcinogenesis was observed
Akt↓, treatment reduced the protein abundance of Akt, Akt1, Akt2, Akt3, phospho-Akt Ser473, phospho-Akt Thr 308, GSK3β, FOXO1, FOXO3a, phospho-FOXO1
GSK‐3β↓,
FOXO3↓,
eff↑, Co-treatment with CAPE and 5-fluorouracil exhibited additive anti-proliferation of TW2.6 cells.
IL2↑, Propolis administration stimulated IL-2 and IL-10 production
IL10↑,
NF-kB↓, reduces the expression of growth and transcription factors, including NF-κB.
VEGF↓, CAPE dose-dependently suppresses vascular endothelial growth factor (VEGF) formation by MDA-231 cells,
mtDam↑, Brazilian red propolis significantly reduced the cancer cell viability through the induction of mitochondrial dysfunction, caspase-3 activity and DNA fragmentation.
ER Stress↑, the action was believed to be due to endoplasmic reticulum stress-related signalling induction of CCAAT/enhancer-binding protein homologous protein (CHOP)
AST↓, Rats,(250 mg/kg) thrice a week for 3 weeks
ALAT↓, Rats,(250 mg/kg) thrice a week for 3 weeks
ALP↓, Rats,(250 mg/kg) thrice a week for 3 weeks
COX2↓, Rats,(250 mg/kg) thrice a week for 3 weeks, Expression of COX-2 and NF-kB p65 was significantly lowered
eff↑, co-treatment of cancer cells with 100 ng/mL TRAIL and 50 μg/mL propolis extract increased the percentage of apoptotic cells to about 66% and caused a significant disruption of membrane potential in LNCaP cells (
Bax:Bcl2↑, decreased Bcl-2/Bax ratio
NF-kB↓, CAPE (a bioactive constituent of propolis) was reported to have anticancer properties by inhibiting NF-κB, caspase and Fas signaling activation in MCF-7 cells
Casp↓,
Fas↓,
DNAdam↑, DNA fragmentation, CCAAT/enhancer binding protein homologous protein expression and caspase-3 activity
Casp3↑,
P53↝, Chinese propolis (EECP) and its bioactive constituents mainly persist due to regulation of the annexin A7 and p53 proteins, mitochondrial membrane potential and ROSs, as well as that inhibition of NF-κB causes apoptosis in cancer cells
MMP↝,
ROS↑, Herrera et al. and reported on the MDA-MB 231 tumor cell line, and the inhibitory effect of propolis was proposed to occur through the induction of mitochondrial dysfunction, resulting in ROS-associated necrosis
mtDam↑,
Dose?, A concentration of 100 μg/mL was able to attain 71% cytotoxicity
angioG↓, negative effect on angiogenesis, proliferation and migration of tumor cells. A concentration of 25–200 μg/mL noticeably inhibited the metastasis of breast cancer
TumCP↓,
TumCMig↓,
BAX↑,
selectivity↑, Negligible effect in fibroblasts
MMP↓, Cuban: Disturbed the mitochondrial potential, lactate dehydrogenase released, production of ROS and cell migration
LDH↓,
IL6↓, Chinese: Decreased cell tube generation, IL-6, IL-1β, TNF-α-like inflammatory mediators, glycolytic enzymes and mitochondrial potential. Promoted ROS generation
IL1β↓,
TNF-α↓,
*antiOx↑, effective antioxidant and anti-inflammatory agent
*Inflam↓,
*toxicity↑, It has been suggested that CAPE, a constituent of propolis, inhibits inducible nitric oxide synthase (iNOS) pathways which may decrease kidney perfusion and thus induce acute renal failure in at-risk patients
*Dose?, a safe dose of propolis has been reported to be 70 mg/day [27]. Interestingly, studies on pinocembrin, a component of propolis, have been conducted using 150 mg as a single dose
ChemoSen↑, Ingredients from propolis also ”sensitize“ cancer cells to chemotherapeutic agents
TumCCA↑, cell-cycle arrest and attenuation of cancer cells proliferation
TumCP↓,
Apoptosis↑,
antiOx↓, behave as antioxidants against peroxyl and hydroxyl radicals,
ROS↑, whereas prooxidant activity is observed in the presence of Cu2+.
COX2↑, Propolis, as well as flavonoids derived from propolis, such as galangin, is a potent COX-2 inhibitor
ER(estro)↓, Some flavonoids from propolis, such as galangin, genistein, baicalein, hesperetin, naringenin, and quercetin, suppressed the proliferation of an estrogen receptor (ER)
cycA1/CCNA1↓, by suppressing expressions of cyclin A, cyclin B, and Cdk2 and by stopping proliferation at the G2 phase, by increasing levels of p21 and p27 proteins, and through the inhibition of telomerase reverse transcriptase (hTERT),
CycB/CCNB1↓,
CDK2↓,
P21↑,
p27↑,
hTERT/TERT↓, leukemia cells, propolis successfully reduced hTERT mRNA expression
HDAC↓, by suppressing expressions of cyclin A, cyclin B, and Cdk2 and by stopping proliferation at the G2 phase, by increasing levels of p21 and p27 proteins, and through the inhibition of telomerase reverse transcriptase (hTERT),
ROS⇅, Mexican propolis, demonstrated both pro- and anti-inflammatory effects, depending on the dose applied
Dose?, Mexican propolis, demonstrated both pro- and anti-inflammatory effects, depending on the dose applied
ROS↓, By scavenging free radicals, chelating metal ions (mainly iron and copper), and stimulating endogenous antioxidant defenses, propolis and its flavonoids directly attenuate the generation of ROS
ROS↑, Romanian propolis [99], exhibits prooxidant properties at high concentrations, by mobilizing endogenous copper ions and DNA-associated copper in cells.
DNAdam↑, propolis, i.e., its polyphenolic components, may induce DNA damage in the presence of transition metal ions.
ChemoSen↑, Algerian propolis + doxorubicin decreased cell viability, prevented cell proliferation and cell cycle progression, induced apoptosis by activating caspase-3 and -9 activities, and increased the accumulation of chemotherapeutic drugs in MDA-MB-231 cel
LOX1↓, propolis components inhibited the LOX pathway
lipid-P↓, Croatian propolis improved psoriatic-like skin lesions induced by irritant agents n-hexyl salicylate or di-n-propyl disulfide by decreasing the extent of lipid peroxidation
NO↑, Taken together, propolis may increase the phagocytic index, NO production, and production of IgG antibodies
Igs↑,
NK cell↑, propolis treatment for 3 days increases the cytotoxic activity of NK cells against murine lymphoma.
MMPs↓, extracts of propolis containing artepillin C and CAPE decreased the formation of new vessels and expression of MMPs and VEGF in various cancer cells
VEGF↓,
Hif1a↓, Brazilian green propolis inhibit the expression of the hypoxia-inducible factor-1 (HIF-1) protein and HIF-1 downstream targets such as glucose transporter 1, hexokinase 2, and VEGF-A
GLUT1↓,
HK2↓,
selectivity↑, Portuguese propolis was selectively toxic against malignant cells.
RadioS↑, propolis increased the lifespan of mice that received the radiotherapy with gamma rays
GlucoseCon↓, Portuguese propolis disturbed the glycolytic metabolism of human colorectal cancer cells, as evidenced by a decrease in glucose consumption and lactate production
lactateProd↓,
eff↓, Furthermore, different pesticides or heavy metals can be found in propolis, which can cause unwanted side effects.
*BioAv↓, Due to the low bioavailability and clinical efficacy of propolis and its flavonoids, their biomedical applications remain limited.
ROS↑, [i.e. focused ultrasound (FUS)] to drive highly localized formation of tumor cell-killing reactive oxygen species (ROS).
eff↑, FUS activates “sonosensitizers”, which like photosensitizers, selectively accumulate in tumor cells and generate ROS.
Dose?, typically 1W/cm2 and up
*Dose?, see description for manufacturing SeNPs
Dose?, see description for method for synthesis
*other↑, human exposure to Si imparts health benefits and essentially occurs through plant-derived food products.
*BMD↑, Si bioavailability in human diet, e.g., strengthens bones and improves immune response, as well as neuronal and connective tissue health.
*Dose↝, It is estimated that human daily intake of Si as silicic acid ranges from 9 to 14 mg, while intakes near 25 mg/d might promote bone health
*cognitive↑, low Si levels in drinking water increase the risk of cognitive impairment due to high aluminum (Al) intake
*Dose?, In order to prevent risks of developing Al-induced Alzheimer’s disease, use of silica rich water with concentrations ≥11 mg/L is recommended
Dose?, coadministration of these vitamins (in a ratio of 100:1, for C and K(3), respectively) produced selective cancer cell death.
TumCD↑,
selectivity↑,
H2O2↑, formation of H(2)O(2) during vitamins redox cycling, oxidative stress, DNA fragmentation
ROS↑,
DNAdam↑,
ROS↑, vitamin K3- or vitamin C- induced apoptosis in leukemia cells by oxidative stress
H2O2↑, hydrogen peroxide generation,
NF-kB↑, activation of NF-κB,
P53↑, p53, c-Jun, protease caspase-3 activation
cJun↑,
Casp3↑,
MMP↓, mitochondria depolarization leading to nuclei fragmentation
DNAdam↑,
Dose?, Jurkat and K562 cells are exposed to VC and VK3 in a ratio 1000:1 (10 mM: 10 μM) or 100:1 (300 μM: 3 μM), respectively
Wmax↑, maximal workload (Wmax) significantly increased
UrinaryC↑, severe urinary incontinence after radical prostatectomy due to prostate cancer. After whole body vibration therapy the patient regained continence,
other↓, authors reported a reduction of the time needed to complete the chair-rising test (CRT)
in the individuals of the WBV group
other↓, "tingling" as well as "discomfort" in the feet of the program Functional Assessment of Cancer Therapy/Gynecologic Oncology Group neurotoxicity subscale (FACT/GOG-NTX) were also significantly lower
Dose?, WBV exercise frequencies ranged from 9 to 50 Hz,
Showing Research Papers: 1 to 34 of 34
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 34
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
antiOx↓, 1, antiOx↑, 2, ENOX2↓, 1, ENOX2↑, 1, GPx1↓, 1, GPx1↑, 1, H2O2↑, 2, lipid-P↓, 1, lipidDe↓, 1, NADH↓, 1, NADHdeh?, 1, ROS↓, 1, ROS↑, 9, ROS⇅, 1, SOD1↓, 1, SOD1↑, 1, SOD2↓, 1, SOD2↑, 1, TrxR↓, 1, TrxR1↓, 1,
Mitochondria & Bioenergetics ⓘ
ATP↓, 1, MEK↓, 1, MMP↓, 5, MMP↝, 1, mtDam↑, 2, Raf↓, 1, XIAP↓, 1,
Core Metabolism/Glycolysis ⓘ
ACLY↓, 2, ALAT↓, 1, AMPK↑, 2, FASN↑, 1, FBPase↑, 1, glucoNG↑, 1, GlucoseCon↓, 1, Glycolysis↓, 3, HK2↓, 1, lactateProd↓, 1, LDH↓, 1, OAA↑, 1, PFK1↓, 1, PFK2↓, 1, p‑S6K↓, 1, TCA↑, 1,
Cell Death ⓘ
Akt↓, 3, p‑Akt↓, 1, Apoptosis↑, 4, BAX↑, 1, Bax:Bcl2↑, 2, Bcl-2↓, 1, Bcl-xL↓, 1, Casp↓, 1, Casp2↑, 1, Casp3↑, 6, Casp8↑, 2, Casp9↑, 2, Chk2↑, 1, DR5↑, 1, Fas↓, 1, hTERT/TERT↓, 1, Mcl-1↓, 1, p27↑, 2, p‑RSK↑, 1, survivin↓, 1, Telomerase↓, 1, TRAILR↑, 1, TumCD↑, 3,
Transcription & Epigenetics ⓘ
cJun↑, 1, ac‑H4↓, 1, other↓, 2, other↑, 2, UrinaryC↑, 1, Wmax↑, 1,
Protein Folding & ER Stress ⓘ
CHOP↑, 1, ER Stress↑, 1, PERK↑, 1,
DNA Damage & Repair ⓘ
CHK1↑, 1, DNAdam↑, 5, DNMTs↓, 1, P53↑, 1, P53↝, 1,
Cell Cycle & Senescence ⓘ
CDK2↓, 2, CDK4↓, 1, cycA1/CCNA1↓, 1, CycB/CCNB1↓, 1, cycD1/CCND1↓, 1, cycE/CCNE↓, 1, P21↑, 1, TumCCA↑, 3,
Proliferation, Differentiation & Cell State ⓘ
CD133↓, 1, CSCs↓, 1, Diff↓, 1, EMT↓, 1, ERK↓, 2, p‑ERK↑, 1, FOXO3↓, 1, GSK‐3β↓, 1, HDAC↓, 2, IGF-1R↓, 1, mTOR↓, 1, p‑mTORC1↓, 1, n-MYC↓, 1, Nestin↓, 1, NOTCH↓, 1, PI3K↓, 2, PTEN↑, 3, p‑PTEN↓, 1, SOX2↓, 1, STAT3↓, 2, TOP1↓, 1, TumCG↓, 2,
Migration ⓘ
Ca+2↑, 1, p‑FAK↑, 1, Ki-67↓, 1, MMP2↓, 2, MMP9↓, 2, MMPs↓, 3, TumCMig↓, 1, TumCMig↑, 1, TumCP↓, 4, TumCP↑, 1, TumMeta↓, 1, uPA↓, 1, α-tubulin↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 3, EGFR↓, 1, Hif1a↓, 2, LOX1↓, 1, NO↑, 1, PHDs↓, 1, VEGF↓, 3, VEGFR2↓, 1,
Barriers & Transport ⓘ
GLUT1↓, 1,
Immune & Inflammatory Signaling ⓘ
CCR7↓, 1, COX2↓, 3, COX2↑, 1, CXCR4↓, 1, Igs↑, 1, IL10↑, 1, IL1β↓, 1, IL2↑, 1, IL6↓, 2, Inflam↓, 3, JAK2↓, 1, MCP1↓, 1, NF-kB↓, 4, NF-kB↑, 1, NK cell↑, 1, PGE2↓, 2, TNF-α↓, 1,
Hormonal & Nuclear Receptors ⓘ
ER(estro)↓, 1,
Drug Metabolism & Resistance ⓘ
ChemoSen↑, 5, Dose?, 27, Dose↓, 1, Dose↑, 2, Dose↝, 1, Dose∅, 4, eff↓, 4, eff↑, 11, eff↝, 3, eff∅, 1, RadioS↑, 4, selectivity↑, 8,
Clinical Biomarkers ⓘ
ALAT↓, 1, ALP↓, 1, AST↓, 1, BG↓, 1, EGFR↓, 1, hTERT/TERT↓, 1, IL6↓, 2, Ki-67↓, 1, LDH↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 2, AntiTum↑, 1, cardioP↑, 1, chemoP↑, 2, ChemoSideEff↓, 1, Risk↓, 2, toxicity↓, 1, TumW↓, 1,
Total Targets: 179
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, ROS↓, 1, ROS↑, 1, ROS⇅, 1,
Core Metabolism/Glycolysis ⓘ
Acetyl-CoA↓, 1, ACLY∅, 1, AMPK↑, 1, CRM↓, 1, SIRT1↑, 1,
Transcription & Epigenetics ⓘ
other↑, 1, other↝, 1,
Proliferation, Differentiation & Cell State ⓘ
mTORC1↓, 1, STAT3↓, 1,
Immune & Inflammatory Signaling ⓘ
IL17↓, 1, IL22↓, 1, Inflam↓, 2, TNF-α↓, 1,
Synaptic & Neurotransmission ⓘ
MAOA↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, BioAv↑, 1, Dose?, 7, Dose↑, 2, Dose↝, 1, Dose∅, 1, eff↑, 1, Half-Life↝, 1,
Clinical Biomarkers ⓘ
BMD↑, 1,
Functional Outcomes ⓘ
AntiAge↑, 2, cognitive↑, 1, toxicity↓, 1, toxicity↑, 2, toxicity↝, 2, toxicity∅, 1,
Infection & Microbiome ⓘ
Bacteria↓, 1,
Total Targets: 34
Scientific Paper Hit Count for: Dose, Dosage
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
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:% Target#:1114 State#:% Dir#:0
wNotes=on sortOrder:rid,rpid
Home Page