ChemoSen Cancer Research Results
ChemoSen, chemo-sensitization: Click to Expand ⟱
| Source: |
| Type: |
The effectiveness of chemotherapy by increasing cancer cell sensitivity to the drugs used to treat them, which is known as “chemo-sensitization”.
Chemo-Sensitizers:
-Curcumin
-Resveratrol
-EGCG
-Quercetin
-Genistein
-Berberine
-Piperine: alkaloid from black pepper
-Ginsenosides: active components of ginseng
-Silymarin
-Allicin
-Lycopene
-Ellagic acid
-caffeic acid phenethyl ester
-flavopiridol
-oleandrin
-ursolic acid
-butein
-betulinic acid
|
Scientific Papers found: Click to Expand⟱
| - |
in-vitro, |
HCC, |
Hep3B |
|
|
|
- |
in-vitro, |
HCC, |
HUH7 |
|
|
|
ChemoSen↓, combination of 2-DG and sorafenib reduced persister tumor growth in mice
Glycolysis↓, The glycolysis inhibitor 2-Deoxy-D-glucose (2-DG), an inhibitor of all forms of HK
HK1↓,
HK2↓,
ATP↓, reducing ATP production
ChemoSen↓, Experiments have shown that allicin can be chemopreventive to gastric cancer
TumCG↓, by inhibiting the growth of cancer cells, arresting cell cycle at G2/M phase, endoplasmic reticulum (ER) stress, and mitochondria-mediated apoptosis, which includes the caspase-dependent/-independent pathways and death receptor pathway.
TumCCA↑,
ER Stress↑,
Apoptosis↑,
Casp↑,
DR5↑, DR5 (death receptor 5) was found to be upregulated following allicin treatment
ChemoSen↓, In this review, the use of antioxidant supplements can benefit cancer cells in the same way as they do for normal cells during cancer treatment.
other↝, Therefore, oncologists should advise not to take antioxidant supplements during chemotherapy and/or radiotherapy.
other↝, Note possible bias in this review, as many of the selenium mega reviews he quotes state there is an improvement, but author rejects as "lack consistent findings"?
eff↓, Taking antioxidants in supplement form (again, remember that antioxidants in food are fine) may actually “protect” cancer cells during treatment.
ChemoSen↓, In other words, antioxidants in pill form have the potential to counteract the effects of chemotherapy or radiation therapy.
RadioS↓,
other↝, Common antioxidant supplements taken by patients include vitamins A, C, and E, carotenoids (such as beta-carotene and lycopene) as well as selenium and Coenzyme Q10.
| - |
in-vitro, |
BC, |
MCF-7 |
|
|
|
- |
in-vitro, |
BC, |
MDA-MB-231 |
|
|
|
eff↓, Berberine Attenuates the Anti-Breast Cancer Activity of Chemotherapeutic Agents
ROS↑, LDB mildly while HDB greatly stimulated ROS generation BBR-induced ROS generation may activate the antioxidant response therefore to promote cancer cell proliferation.
TumCP↑,
NRF2↑,
ChemoSen↓, These findings revealed a potential negative impact of BBR on its adjuvant anti-breast cancer therapy
| - |
in-vitro, |
CRC, |
SW480 |
|
|
|
- |
in-vitro, |
CRC, |
HCT116 |
|
|
|
ChemoSen↓, We observed that the addition of CAPE significantly augmented the drug sensitivity of colon cancer cells to oxaliplatin.
Apoptosis↑, The combination of OXA and CAPE enhanced apoptosis induction in colon cancer cells compared with treatment with OXA alone,
ChemoSen↓, Our findings suggest that coenzyme Q10 increase is implicated in the cellular defense under chemotherapy treatment and may contribute to cell survival.
*antiOx↑, CoQ also functions as an antioxidant which protects the cells both directly by preventing lipid peroxidation
*lipid-P?,
AntiCan↑, dependence of many tumor cells on an exogenous source of the sulfur amino acid, methionine, [9,10,11] makes dietary methionine restriction (MR) an exciting potential tool in the treatment of cancer.
TumCP↓, Proliferation and growth of several types of cancer cells are inhibited by MR,
TumCG↓,
selectivity↑, while normal cells are unaffected by limiting methionine as long as homocysteine is present
ChemoSen↓, MR has been shown to enhance efficacy of chemotherapy and radiation therapy in animal models
RadioS↑,
Insulin↓, MR may work by inhibiting prostate cancer cell proliferation, inhibiting the insulin/IGF-1 axis
*GlucoseCon↑, increase in tissue-specific glucose uptake measured during a hyperinsulinemic-euglycemic clamp
*ROS↓, MR does not increase oxidative stress, in part because MR enhances antioxidant capacity and increases proton leak in the liver, likely decreasing ROS production
*antiOx↑,
*GSH↑, ability of MR to increase GSH levels in red blood cells. Surprisingly, when methionine was restricted by 80% in the diet of rats, the level of GSH in the blood actually increased due to adaptations in sulfur-amino acid metabolism
GSH↑, However, GSH concentrations were reduced in the liver
eff↑, Of note, methionine restriction is effective when the non-essential amino acid, cysteine, is absent from the diet or media.
polyA↓, MR may work by inhibiting prostate cancer cell proliferation, inhibiting the insulin/IGF-1 axis, or by reducing polyamine synthesis. MR-induced depletion of polyamines
TS↓, MR selectively reduces TS activity in prostate cancer cells by ~80% within 48 h, but does not affect TS activity in normal prostate epithelial cells
Raf↓, MR inhibits Raf and Akt oncogenic pathways, while increasing caspase-9 and the mitochondrial pro-apoptotic protein, Bak
Akt↓,
Casp9↑,
Bak↑,
P21↑, MR upregulating p21 and p27 (cell cycle inhibitors that halt cell cycle progression) in LNCaP cells
p27↑,
Insulin↓, MR-induced reduction in circulating insulin and IGF1, which have both been linked to tumor growth
IGF-1↓,
*antiOx↑, As an antioxidant, Luteolin and its glycosides can scavenge free radicals caused by oxidative damage and chelate metal ions
*IronCh↑,
*toxicity↓, The safety profile of Luteolin has been proven by its non-toxic side effects, as the oral median lethal dose (LD50) was found to be higher than 2500 and 5000 mg/kg in mice and rats, respectively, equal to approximately 219.8−793.7 mg/kg in humans
*BioAv↓, One major problem related to the use of flavonoids for therapeutic purposes is their low bioavailability.
*BioAv↑, Resveratrol, which functions as the inhibitor of UGT1A1 and UGT1A9, significantly improved the bioavailability of Luteolin by decreasing the major glucuronidation metabolite in rats
DNAdam↑, Luteolin’s anticancer properties, which involve DNA damage, regulation of redox, and protein kinases in inhibiting cancer cell proliferation
TumCP↓,
DR5↑, Luteolin was discovered to promote apoptosis of different cancer cells by increasing Death receptors, p53, JNK, Bax, Cleaved Caspase-3/-8-/-9, and PARP expressions
P53↑,
JNK↑,
BAX↑,
cl‑Casp3↑,
cl‑Casp8↑,
cl‑Casp9↑,
cl‑PARP↑,
survivin↓, downregulating proteins involved in cell cycle progression, including Survivin, Cyclin D1, Cyclin B, and CDC2, and upregulating p21
cycD1/CCND1↓,
CycB/CCNB1↓,
CDC2↓,
P21↑,
angioG↓, suppress angiogenesis in cancer cells by inhibiting the expression of some angiogenic factors, such as MMP-2, AEG-1, VEGF, and VEGFR2
MMP2↓,
AEG1↓,
VEGF↓,
VEGFR2↓,
MMP9↓, inhibit metastasis by inhibiting several proteins that function in metastasis, such as MMP-2/-9, CXCR4, PI3K/Akt, ERK1/2
CXCR4↓,
PI3K↓,
Akt↓,
ERK↓,
TumAuto↑, can promote the conversion of LC3B I to LC3B II and upregulate Beclin1 expression, thereby causing autophagy
LC3B-II↑,
EMT↓, Luteolin was identified to suppress the epithelial to mesenchymal transition by upregulating E-cadherin and downregulating N-cadherin and Wnt3 expressions.
E-cadherin↑,
N-cadherin↓,
Wnt↓,
ROS↑, DNA damage that is induced by reactive oxygen species (ROS),
NICD↓, Luteolin can block the Notch intracellular domain (NICD) that is created by the activation of the Not
p‑GSK‐3β↓, Luteolin can inhibit the phosphorylation of the GSK3β induced by Wnt, resulting in the prevention of GSK3β inhibition
iNOS↓, Luteolin in colon cancer and the complications associated with it, particularly the decreasing effect on the expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2)
COX2↓,
NRF2↑, Luteolin has been identified to increase the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), which is a crucial transcription factor with anticarcinogenic properties related
Ca+2↑, caused loss of the mitochondrial membrane action potential, enhanced levels of mitochondrial calcium (Ca2+),
ChemoSen↑, Luteolin enhanced the effect of one of the most effective chemotherapy drugs, cisplatin, on CRC cells
ChemoSen↓, high dose of Luteolin application negatively affected the oxaliplatin-based chemotherapy in a p53-dependent manner [52]. They suggested that the flavonoids with Nrf2-activating ability might interfere with the chemotherapeutic efficacy of anticancer
IFN-γ↓, decreased the expression of interferon-gamma-(IFN-γ)
RadioS↑, suggested that Luteolin can act as a radiosensitizer, promoting apoptosis by inducing p38/ROS/caspase cascade
MDM2↓, Luteolin treatment was associated with increased p53 and p21 and decreased MDM4 expressions both in vitro and in vivo.
NOTCH1↓, Luteolin suppressed the growth of lung cancer cells, metastasis, and Notch-1 signaling pathway
AR↓, downregulating the androgen receptor (AR) expression
TIMP1↑, Luteolin inhibits the migration of U251MG and U87MG human glioblastoma cell lines by downregulating MMP-2 and MMP-9 and upregulating the tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2.
TIMP2↑,
ER Stress↑, Luteolin caused oxidative stress and ER stress in the Hep3B cells,
CDK2↓, Luteolin’s ability to decrease Akt, polo-like kinase 1 (PLK1), cyclin B1, cyclin A, CDC2, cyclin-dependent kinase 2 (CDK2) and Bcl-xL
Telomerase↓, Luteolin dose-dependently inhibited the telomerase levels and caused the phosphorylation of NF-κB and the target gene of NF-κB, c-Myc to suppress the human telomerase reverse transcriptase (hTERT)
p‑NF-kB↑,
p‑cMyc↑,
hTERT/TERT↓,
RAS↓, Luteolin was found to suppress the expressions of K-Ras, H-Ras, and N-Ras, which are the activators of PI3K
YAP/TEAD↓, Luteolin caused significant inhibition of yes-associated protein (YAP)/transcriptional co-activator with PDZ-binding motif (TAZ)
TAZ↓,
NF-kB↓, Luteolin was found to have a strong inhibitory effect on the NF-κB
NRF2↓, Luteolin-loaded nanoparticles resulted in a significant reduction in the Nrf2 levels compared to Luteolin alone.
HO-1↓, The expressions of the downstream genes of Nrf2, Ho1, and MDR1 were also reduced, where inhibition of Nrf2 expression significantly increased the cell death of breast cancer cells
MDR1↓,
antiOx↑, lycopene supplementation is associated with strong antioxidant effects, it has the potential to interfere with chemotherapy and radiation therapy
ChemoSen↓,
RadioS↓,
AntiCan↑, Sodium Bicarbonate “Kills” Cancer Cells
e-pH↑, The utilization of sodium bicarbonate to neutralize the acidity and increase the tumor pHe might control cancer cells progression
TumMeta↓, Sodium bicarbonate reduces the formation of spontaneous metastases and the rate of lymph node involvement in mouse models of metastatic breast cancer.
TumCI↓, administration of 200 mM bicarbonate to 4-week-old TRAMP mice (weaning at 3 weeks) effectively perturbs the in situ evolution of cancer to a microinvasive disease
TumCG↓, sodium bicarbonate significantly controls tumor growth and improves CD8+ T-cell infiltration.
CD8+↑,
NK cell↑, Natural killer (NK) cell activity is also increased in a B-cell lymphoma mouse model following the systemic administration of a buffer therapy.
Remission↑, began a self-administered course of vitamins, supplements, and 60 g of bicarbonate mixed in water daily. As of this submission, he has remained well with stable tumor for 10 months.
eff↑, Therefore, sodium bicarbonate could be used as an adjuvant therapy to enhance the efficacy of conventional treatments.
ChemoSen↑, Surprisingly, extracellular alkalization induced a 2- to 3-fold increase in the efficacy of doxorubicin
ChemoSen↓, it greatly reduces the efficacy of some weak acidic chemotherapeutics, such as chlorambucil.
ChemoSen↓, 4 human clinical trials that demonstrated the successful use of propolis in alleviating side effects of chemotherapy and radiotherapy while increasing the quality of life of breast cancer patients, with minimal adverse effects.
RadioS↑,
Inflam↓, immunomodulatory, anti-inflammatory, and anti-cancer properties.
AntiCan↑,
Dose∅, Indonesia: IC50 = 4.57 μg/mL and 10.23 μg/mL
mtDam↑, Poland: propolis induced mitochondrial damage and subsequent apoptosis in breast cancer cells.
Apoptosis?,
OCR↓, China: CAPE inhibited mitochondrial oxygen consumption rate (OCR) by reducing basal, maximal, and spare respiration rate and consequently inhibiting ATP production
ATP↓,
ROS↑, Iran: inducing intracellular ROS production, IC50 = 65-96 μg/mL
ROS↑, Propolis induced mitochondrial dysfunction and lactate dehydrogenase release indicating the occurrence of ROS-associated necrosis.
LDH↓,
TP53↓, Interestingly, a reduced expression of apoptosis-related genes such as TP53, CASP3, BAX, and P21)
Casp3↓,
BAX↓,
P21↓,
ROS↑, CAPE: inducing oxidative stress through upregulation of e-NOS and i-NOS levels
eNOS↑,
iNOS↑,
eff↑, The combination of propolis and mangostin significantly reduced the expression of Wnt2, FAK, and HIF-1α, when compared to propolis or mangostin alone
hTERT/TERT↓, downregulation of the mRNA levels of hTERT and cyclin D1
cycD1/CCND1↓,
eff↑, Synergism with bee venom was observed
eff↑, Statistically significant decrease was found in the MCF-7 cell viability 48 h after applying different combinations of cisplatin (3.12 μg/mL) and curcumin (0.31 μg/mL) and propolis (160 μg/mL)
eff↑, Nanoparticles of chrysin had significantly higher cytotoxicity against MCF-7 cells, compared to chrysin
eff↑, Propolis nanoparticles appeared to increase cytotoxicity of propolis against MCF-7 cells
STAT3↓, Chrysin also inhibited the hypoxia-induced STAT3 tyrosine phosphorylation suggesting the mechanism of action was through STAT3 inhibition.
TIMP1↓, Propolis reduced the expression of TIMP-1, IL-4, and IL-10.
IL4↓,
IL10↓,
OS↑, patients supplemented with propolis had significantly longer median disease free survival time (400 mg, 3 times daily for 10 d pre-, during, and post)
Dose∅, 400 mg, 3 times daily for 10 d pre-, during, and post
ER Stress↑, endoplasmic reticulum stress
ROS↑, upregulating the expression of Annexin A7 (ANXA7), reactive oxygen species (ROS) level, and NF-κB p65 level, while simultaneously reducing the mitochondrial membrane potential.
NF-kB↓,
p65↓,
MMP↓,
TumAuto↑, propolis induced autophagy by increasing the expression of LC3-II and reducing the expression of p62 level
LC3II↑,
p62↓,
TLR4↓, propolis downregulates the inflammatory TLR4
mtDam↑, propolis induced mitochondrial dysfunction and lactate dehydrogenase release indicating ROS-associated necrosis in MDA MB-231cancer cells
LDH↓,
ROS↑,
Glycolysis↓, inhibit the proliferation of MDA-MB-231 cells by targeting key enzymes of glycolysis, namely glycolysis-hexokinase 2 (HK2), phosphofructokinase (PFK), pyruvate kinase muscle isozyme M2 (PKM2), and lactate dehydrogenase A (LDHA),
HK2↓,
PFK↓,
PKM2↓,
LDH↓,
IL10↓, propolis significantly reduced the relative number of CD4+, CD25+, FoxP3+ regulatory T cells expressing IL-10
HDAC8↓, Chrysin, a propolis bioactive compound, inhibits HDAC8
eff↑, combination of propolis and mangostin significantly reduced the expression of Wnt2, FAK, and HIF-1α, when compared to propolis or mangostin alone.
eff↑, Propolis also upregulated the expression of catalase, HTRA2/Omi, FADD, and TRAIL-associated DR5 and DR4 which significantly enhanced the cytotoxicity of doxorubicin in MCF-7 cells
P21↑, Chrysin, a propolis bioactive compound, inhibits HDAC8 and significantly increases the expression of p21 (waf1/cip1) in breast cancer cells, leading to apoptosis.
ChemoSen↓, Chemosensitization by TQ is mostly limited to in vitro studies, and it has potential in therapeutic strategy for cancer
*ROS↓, its scavenging ability against freeradicals, including reactive oxygen species (ROS;
*GSH↑, TQ reduces the cellular oxidative stress by inducing glutathione (GSH)
RenoP↑, TQ protects the kidney against ifosfamide, mercuric chloride, cisplatin, and doxorubicin-induced damage by preventing renal GSH depletion and antilipid peroxidation
hepatoP↑, TQ ameliorated hepatotoxicity of
carbon tetrachloride as seen by the significant reduction of the
elevated levels of serum enzymes and significant increase of the
hepatic GSH content
COX2↓, TQ induces inhibition of PGE2 and COX-2, in a COX-2 overexpressing HPAC cells (PC cells).
NF-kB↓, NF-κB is a molecular target of TQ in cance
chemoPv↑, TQ is a chemopreventive agent for prostate cancer
neuroP↑, The beneficial effect of TQ as a neuroprotective agent in inhibiting viability of human neuroblastoma cell line SH-SY5Y
TumCCA↑, TQ, it reportedly induces G1 cell cycle arrest in osteosarcoma cancer cells (COS31) as well as in human colon
cancer cells (HCT-116),
P21↑, TQ caused a dramatic increase in p21WAF1 , (Cip1), and p27 (Kip1) and blocked the progression of synchronized LNCaP cells from G1 to S phase,
p27↑,
ROS↑, TQ on p53 deficient lymphoblastic leukemia Jurkat cells and found TQ treatment produced intracellular ROS pro-
moting a DNA damage-related cell cycle arrest and triggered apoptosis
DNAdam↑,
MUC4↓, in pancreatic cancer cells and it was found that TQ downregulates MUC-4 expression through the proteasomal pathway
TumCP↓, Exposure to urolithin A also dose‐dependently decreased cell proliferation, delayed cell migration, and decreased matrix metalloproteinas‐9 (MMP‐9) activity.
TumCMig↓,
MMP9↓,
TumAuto↑, Micromolar urolithin A concentrations induced both autophagy and apoptosis.
Apoptosis↑,
TumCCA↓, Urolithin A suppressed cell cycle progression and inhibited DNA synthesis.
TumMeta↓, dietary consumption of urolithin A could induce autophagy and inhibit human CRC cell metastasis.
ChemoSen↓, offer an alternative or adjunct chemotherapeutic agent to combat this disease.
TumCCA↑, involving cell-cycle arrest
Apoptosis↑, apoptosis, autophagy and invasion
TumAuto↑,
TumCI↓,
TumCG↓, inhibit the growth of cancer cells
ChemoSen↓, combination treatment of VK2 and established chemotherapeutics may achieve better results, with fewer side effects
ChemoSideEff↓,
toxicity∅, VK2 is milder, but causes no side effects, whereas VK1 has the least strong function
eff↑, combination of VK2 and vitamin E suppressed the growth of the primary tumor and obliterated the intraperitoneal dissemination in a 65-year-old man with ruptured HCC
cycD1/CCND1↓, decreases in cyclin D1 and cyclin-dependent kinase 4 (CDK4) levels
CDK4↓,
eff↑, pretreatment with VK2 prior to sorafenib treatment is proven to exert more effective HCC growth inhibition in animals than treatment with either alone
IKKα↓, VK2 can inhibit the IκB kinase (IKK)/IκB/NF-κB pathway
NF-kB↓,
other↑, stimulate the phosphorylation of PKA and activate activating protein 2 (AP-2)
p27↑, VK2 upregulates the expression of p27
cMyc↓, 5 µΜ VK2 exposure inhibited c-MYC expression in HL-60 leukemia cells
i-ROS↑, VK2 treatment increased the intracellular level of the reactive oxygen species (ROS)
Bcl-2↓, VK2 decreases Bcl-2 expression and increases the expression of Bcl-2-associated X protein (Bax)
BAX↑,
p38↑, VK2 activates p38 MAPK to its phosphorylated form
MMP↓, mitochondrial membrane potential was depolarized and caspase-9 was activated
Casp9↑,
p‑ERK↓, VK2 is reported to inhibit ERK phosphorylation by suppressing Ras activation
RAS↓,
MAPK↓, subsequently suppressing the activation of MAPK kinase (MEK)
p‑P53↑, VK2 stimulated the extrinsic apoptosis pathway by increasing p53 phosphorylation
Casp8↑, caspase-8 activation and further activates caspase-3
Casp3↑,
cJun↑, increasing the expression of c-JUN and c-MYC;
MMPs↓, downregulating the expression of matrix metalloproteinases (MMPs)
eff↑, combination of VK2 with other chemotherapy agents can produce stronger effects than the use of either alone
eff↑, combination of vitamin D3 with VK2 on cancer cells can synergistically improve the induction of cellular differentiation and also significantly reduces the risk of hypercalcemia and vascular calcification
Showing Research Papers: 1 to 15 of 15
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 15
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, GSH↑, 1, HK1↓, 1, HO-1↓, 1, NRF2↓, 1, NRF2↑, 2, ROS↑, 8, i-ROS↑, 1,
Mitochondria & Bioenergetics ⓘ
ATP↓, 2, CDC2↓, 1, Insulin↓, 2, MMP↓, 2, mtDam↑, 2, OCR↓, 1, Raf↓, 1,
Core Metabolism/Glycolysis ⓘ
cMyc↓, 1, p‑cMyc↑, 1, Glycolysis↓, 2, HK2↓, 2, LDH↓, 3, PFK↓, 1, PKM2↓, 1, polyA↓, 1, TS↓, 1,
Cell Death ⓘ
Akt↓, 2, Apoptosis?, 1, Apoptosis↑, 4, Bak↑, 1, BAX↓, 1, BAX↑, 2, Bcl-2↓, 1, Casp↑, 1, Casp3↓, 1, Casp3↑, 1, cl‑Casp3↑, 1, Casp8↑, 1, cl‑Casp8↑, 1, Casp9↑, 2, cl‑Casp9↑, 1, DR5↑, 2, hTERT/TERT↓, 2, iNOS↓, 1, iNOS↑, 1, JNK↑, 1, MAPK↓, 1, MDM2↓, 1, NICD↓, 1, p27↑, 3, p38↑, 1, survivin↓, 1, Telomerase↓, 1, YAP/TEAD↓, 1,
Transcription & Epigenetics ⓘ
cJun↑, 1, other↑, 1, other↝, 3,
Protein Folding & ER Stress ⓘ
ER Stress↑, 3,
Autophagy & Lysosomes ⓘ
LC3B-II↑, 1, LC3II↑, 1, p62↓, 1, TumAuto↑, 4,
DNA Damage & Repair ⓘ
DNAdam↑, 2, P53↑, 1, p‑P53↑, 1, cl‑PARP↑, 1, TP53↓, 1,
Cell Cycle & Senescence ⓘ
CDK2↓, 1, CDK4↓, 1, CycB/CCNB1↓, 1, cycD1/CCND1↓, 3, P21↓, 1, P21↑, 4, TumCCA↓, 1, TumCCA↑, 3,
Proliferation, Differentiation & Cell State ⓘ
EMT↓, 1, ERK↓, 1, p‑ERK↓, 1, p‑GSK‐3β↓, 1, HDAC8↓, 1, IGF-1↓, 1, NOTCH1↓, 1, PI3K↓, 1, RAS↓, 2, STAT3↓, 1, TAZ↓, 1, TumCG↓, 4, Wnt↓, 1,
Migration ⓘ
AEG1↓, 1, Ca+2↑, 1, E-cadherin↑, 1, MMP2↓, 1, MMP9↓, 2, MMPs↓, 1, MUC4↓, 1, N-cadherin↓, 1, TIMP1↓, 1, TIMP1↑, 1, TIMP2↑, 1, TumCI↓, 2, TumCMig↓, 1, TumCP↓, 3, TumCP↑, 1, TumMeta↓, 2,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, eNOS↑, 1, VEGF↓, 1, VEGFR2↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, CXCR4↓, 1, IFN-γ↓, 1, IKKα↓, 1, IL10↓, 2, IL4↓, 1, Inflam↓, 1, NF-kB↓, 4, p‑NF-kB↑, 1, NK cell↑, 1, p65↓, 1, TLR4↓, 1,
Cellular Microenvironment ⓘ
e-pH↑, 1,
Hormonal & Nuclear Receptors ⓘ
AR↓, 1,
Drug Metabolism & Resistance ⓘ
ChemoSen↓, 15, ChemoSen↑, 2, Dose∅, 2, eff↓, 2, eff↑, 13, MDR1↓, 1, RadioS↓, 2, RadioS↑, 3, selectivity↑, 1,
Clinical Biomarkers ⓘ
AR↓, 1, hTERT/TERT↓, 2, LDH↓, 3, TP53↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 3, chemoPv↑, 1, ChemoSideEff↓, 1, hepatoP↑, 1, neuroP↑, 1, OS↑, 1, Remission↑, 1, RenoP↑, 1, toxicity∅, 1,
Infection & Microbiome ⓘ
CD8+↑, 1,
Total Targets: 143
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 3, GSH↑, 2, lipid-P?, 1, ROS↓, 2,
Metal & Cofactor Biology ⓘ
IronCh↑, 1,
Core Metabolism/Glycolysis ⓘ
GlucoseCon↑, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, BioAv↑, 1,
Functional Outcomes ⓘ
toxicity↓, 1,
Total Targets: 9
Scientific Paper Hit Count for: ChemoSen, chemo-sensitization
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#:1106 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
Home Page