TumCMig Cancer Research Results
TumCMig, Tumor cell migration: Click to Expand ⟱
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Tumor cell migration is a critical process in cancer progression and metastasis, which is the spread of cancer cells from the primary tumor to distant sites in the body.
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Scientific Papers found: Click to Expand⟱
TrxR↓, Auranofin (AUR), a thioredoxin reductase (TXNRD) inhibitor, shows anticancer activity against several cancers.
ROS↑, AUR induced apoptosis of OS cells via the oxidative stress-MAPK-Caspase 3 pathway, and suppressed the migration of OS cells.
TumCMig↓,
TumCMig↓,
TumCI↓,
Ki-67↓,
TumCP↓,
Snail↓,
Vim↓,
E-cadherin↑,
Wnt↓,
β-catenin/ZEB1↓,
*Imm↑, AR possesses various biological functions, including potent immunomodulation, antioxidant, anti-inflammation and antitumor
activities.
*antiOx↑,
*Inflam↓,
AntiTum↑,
eff↑, characteristics of increasing curative effect and reducing the toxicity of chemotherapeutic drugs [11 , 118].
chemoP↑,
Dose↝, main bioactive compounds responsible for the anti-cancer effects of AR mainly include formononetin,
AS-IV and APS. S
TumCMig↓, AS-IV could inhibit the migration and proliferation of non-small cell lung cancer (NSCLC
TumCP↓,
Akt↓, h via inhibition of the Akt/GSK-3β/β-catenin
signaling axis.
GSK‐3β↓,
MMP2↓, downregulating the expression of matrix metalloproteases (MMP)-2 and -9
MMP9↓,
EMT↓, AS-IV could inhibit TGF-B1 induced EMT through inhibition of PI3K/AKT/NF-KB
PI3K↓,
Akt↓,
NF-kB↓,
Inflam↓,
TGF-β1↓,
TNF-α↓,
IL6↓,
Fas↓, reduced FAS/FasL
FasL↓,
NOTCH1↓, decressing notch1
JNK↓, inactivating JNK pathway [145]
TumCG↓, The results showed that the AR water extract could inhibit the growth of colorectal cancer in vivo without apparent toxicity and side effect, which suggests that AR is a potential therapeutic drug for colorectal cancer
other↓, Combined STM2457 and APS treatment significantly reduced m6A levels, METTL3, HNRNPA2B1, and FOXQ1 expression, and mRNA stability compared to single-drug treatments, approaching or surpassing METTL3 silencing effects.
TumCP↓, The combination markedly suppressed cell proliferation, migration, invasion, and EMT, with increased E-cadherin and decreased N-cadherin levels.
TumCMig↓,
TumCI↓,
EMT↓,
E-cadherin↑,
N-cadherin↓,
TumCG↓, In vivo, combination therapy significantly reduced tumor growth and FOXQ1 expression, outperforming single-drug treatments.
TumCP↓, combination markedly suppressed cell proliferation, migration, invasion, and EMT, with increased E-cadherin and decreased N-cadherin levels.
TumCMig↓,
TumCI↓,
EMT↓,
E-cadherin↑,
N-cadherin↓,
TumCMig↓, Our results showed that C-AgNPs significantly inhibited MCF-7 cell migration
Apoptosis↑, gene expression analysis indicated the induction of apoptosis by upregulation of pro-apoptotic genes BAX and P53 and downregulation of Bcl-2.
BAX↑,
P53↑,
Bcl-2↓,
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in-vitro, |
Lung, |
A549 |
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in-vitro, |
Liver, |
HepG2 |
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*Bacteria↓, silver nanoparticles synthesized from Dendropanax morbifera Léveille leaves (D-AgNPs) exhibit antimicrobial activity and reduce the viability of cancer cells without affecting the viability of RAW 264.7 macrophage-like cells
tumCV↓,
selectivity↑,
ROS↑, enhanced the production of ROS in both cell lines.
Apoptosis↑, An increase in cell apoptosis and a reduction in cell migration in A549 cells were also observed after D-AgNP treatment.
TumCMig↓,
AntiCan↑, potential of D-AgNPs as a possible anticancer agent, particularly for the treatment of non-small cell lung carcinoma.
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.
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vitro+vivo, |
Bladder, |
5637 |
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TumCD↑, 57% tumor regression
Apoptosis↑,
TumCMig↓,
TumCP↓,
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in-vitro, |
Lung, |
A549 |
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in-vitro, |
Nor, |
HEK293 |
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Casp3↑,
Casp9↑,
P53↑,
ROS↑,
MMP2↓,
MMP9↓,
TumCCA↑, cessation in the G0/G1 phase
*toxicity↓, 9.87ug/ml(cancer cells) and 111.26 µg/ml(normal cells)
TumCMig↓,
TumCI↓,
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in-vitro, |
Cerv, |
HeLa |
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in-vitro, |
BC, |
MDA-MB-231 |
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Vim↑, Surprisingly, and apparently contradictory to the role that vimentin plays in metastasis, a time-dependent increase in total vimentin protein was observed
TumCI↓, Ajoene inhibits invasion and migration
TumCMig↓,
TumMeta↓, offer protection against metastatic cancer, mediated through binding to the vimentin target.
Vim↓, our vimentin finding is therefore the second example in the literature, where ajoene has been found to target and inhibit a protein, with a simultaneous increase in its expression.
other↝, We argue that ajoenes increased vimentin expression may be a response to restore the malfunctioning vimentin network.
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Review, |
AD, |
NA |
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Review, |
Var, |
NA |
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Review, |
Park, |
NA |
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Review, |
Stroke, |
NA |
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*Inflam↓, It showed neuroprotective effects, exhibited anti-inflammatory properties, demonstrated anticancer activity, acted as an antioxidant, provided cardioprotection, exerted antidiabetic effects, and offered hepatoprotection.
AntiCan↑,
*antiOx↑,
*cardioP↑, This vasodilatory effect helps protect against cardiovascular diseases by reducing the risk of hypertension and atherosclerosis.
*hepatoP↑,
*BBB↑, This allows allicin to easily traverse phospholipid bilayers and the blood-brain barrier
*Half-Life↝, biological half-life of allicin is estimated to be approximately one year at 4°C. However, it should be noted that its half-life may differ when it is dissolved in different solvents, such as vegetable oil
*H2S↑, allicin undergoes metabolism in the body, leading to the release of hydrogen sulfide (H2S)
*BP↓, H2S acts as a vasodilator, meaning it relaxes and widens blood vessels, promoting blood flow and reducing blood pressure.
*neuroP↑, It acts as a neuromodulator, regulating synaptic transmission and neuronal excitability.
*cognitive↑, Studies have suggested that H2S may enhance cognitive function and protect against neurodegenerative diseases like Alzheimer's and Parkinson's by promoting neuronal survival and reducing oxidative stress.
*neuroP↑, various research studies suggest that the neuroprotective mechanisms of allicin can be attributed to its antioxidant and anti-inflammatory properties
*ROS↓,
*GutMicro↑, may contribute to the overall health of the gut microbiota.
*LDH↓, Liu et al. found that allicin treatment led to a significant decrease in the release of lactate dehydrogenase (LDH),
*ROS↓, allicin's capacity to lower the production of reactive oxygen species (ROS), decrease lipid peroxidation, and maintain the activities of antioxidant enzymes
*lipid-P↓,
*antiOx↑,
*other↑, allicin was found to enhance the expression of sphingosine kinases 2 (Sphk2), which is considered a neuroprotective mechanism in ischemic stroke
*PI3K↓, allicin downregulated the PI3K/Akt/nuclear factor-kappa B (NF-κB) pathway, inhibiting the overproduction of NO, iNOS, prostaglandin E2, cyclooxygenase-2, interleukin-6, and tumor necrosis factor-alpha induced by interleukin-1 (IL-1)
*Akt↓,
*NF-kB↓,
*NO↓,
*iNOS↓,
*PGE2↓,
*COX2↓,
*IL6↓,
*TNF-α↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
*MPO↓, Furthermore, allicin significantly decreased tumor necrosis factor-alpha (TNF-α) levels and myeloperoxidase (MPO) activity, indicating its neuroprotective effect against brain ischemia via an anti-inflammatory pathway
*eff↑, Allicin, in combination with melatonin, demonstrated a marked reduction in the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2), Kelch-like ECH-associated protein 1 (Keap-1), and NF-κB genes in rats with brain damage induced by acryl
*NRF2↑, Allicin treatment decreased oxidative stress by upregulating Nrf2 protein and downregulating Keap-1 expression.
*Keap1↓,
*TBARS↓, It significantly reduced myeloperoxidase (MPO) and thiobarbituric acid reactive substances (TBARS) levels,
*creat↓, and decreased blood urea nitrogen (BUN), creatinine, LDH, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and malondialdehyde (MDA) levels.
*LDH↓,
*AST↓,
*ALAT↓,
*MDA↓,
*SOD↑, Allicin also increased the activity of superoxide dismutase (SOD) as well as the levels of glutathione S-transferase (GST) and glutathione (GSH) in the liver, kidneys, and brain
*GSH↑,
*GSTs↑,
*memory↑, Allicin has demonstrated its ability to improve learning and memory deficits caused by lead acetate injury by promoting hippocampal astrocyte differentiation.
chemoP↑, Allicin safeguards mitochondria from damage, prevents the release of cytochrome c, and decreases the expression of pro-apoptotic factors (Bax, cleaved caspase-9, cleaved caspase-3, and p53) typically activated by cisplatin
IL8↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
Cyt‑c↑, In addition, allicin was reported to induce cytochrome c, increase expression of caspase 3 [86], caspase 8, 9 [82,87], caspase 12 [80] along with enhanced p38 protein expression levels [81], Fas expression levels [82].
Casp3↑,
Casp8↑,
Casp9↑,
Casp12↑,
p38↑,
Fas↑,
P53↑, Also, significantly increased p53, p21, and CHK1 expression levels decreased cyclin B after allicin treatment.
P21↑,
CHK1↓,
CycB/CCNB1↓,
GSH↓, Depletion of GSH and alterations in intracellular redox status have been found to trigger activation of the mitochondrial apoptotic pathway was the antiproliferative function of allicin
ROS↑, Hepatocellular carcinoma (HCC) cells were sensitised by allicin to the mitochondrial ROS-mediated apoptosis induced by 5-fluorouracil
TumCCA↑, According to research findings, allicin has been shown to decrease the percentage of cells in the G0/G1 and S phases [87], while causing cell cycle arrest at the G2/M phase
Hif1a↓, Allicin treatment was found to effectively reduce HIF-1α protein levels, leading to decreased expression of Bcl-2 and VEGF, and suppressing the colony formation capacity and cell migration rate of cancer cells
Bcl-2↓,
VEGF↓,
TumCMig↓,
STAT3↓, antitumor properties of allicin have been attributed to various mechanisms, including promotion of apoptosis, inhibition of STAT3 signaling
VEGFR2↓, suppression of VEGFR2 and FAK phosphorylation
p‑FAK↓,
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in-vitro, |
BC, |
MDA-MB-231 |
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TumCMig↓,
ERK↓, Allicin suppressed TNF-α-induced activation of ERK1/2
VCAM-1↓,
NF-kB↓,
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in-vitro, |
Pca, |
22Rv1 |
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in-vitro, |
Pca, |
C4-2B |
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in-vitro, |
Nor, |
3T3 |
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tumCV↓, Notably, α‑LA treatment significantly reduced the cell viability, migration, and invasion of PCa cell lines in a dose‑dependent manner.
TumCMig↓,
TumCI↓,
ROS↑, α‑LA supplementation dramatically increased reactive oxygen species (ROS) levels and HIF‑1α expression, which started the downstream molecular cascade and activated JNK/caspase‑3 signaling pathway
Hif1a↑, The expression of HIF-1α significantly increased following α-LA treatment and was comparable
with the changes in ROS.
JNK↑,
Casp↑,
TumCCA↑, arrest of the cell cycle in the S‑phase, which has led to apoptosis
of PCa cells
Apoptosis↑,
selectivity↑, Also, the treatment of α‑LA improved bone health by reducing PCa‑mediated bone cell
modulation.
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in-vitro, |
Bladder, |
T24/HTB-9 |
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ITGB1↓,
TumCMig↓,
ERK↓,
Akt↓,
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Review, |
BC, |
SkBr3 |
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Review, |
neuroblastoma, |
SK-N-SH |
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Review, |
AD, |
NA |
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PDH↑, ALA is capable of activating pyruvate dehydrogenase in tumor cells.
TumCG↓, ALA also significantly inhibited tumor growth in mouse xenograft model using BCPAP and FTC-133 cells
ROS↑, ALA is able to generate ROS, which promote ALA-dependent cell death in lung cancer [75], breast cancer [76] and colon cancer
AMPK↑,
EGR4↓,
Half-Life↓, Data suggests that ALA has a short half-life and bioavailability (about 30%)
BioAv↝,
*GSH↑, Moreover, it is able to increase the glutathione levels inside the cells, that chelate and excrete a wide variety of toxins, especially toxic metals from the body
*IronCh↑, The existence of thiol groups in ALA is responsible for its metal chelating abilities [14,35].
*ROS↓, ALA exerts a direct impact in oxidative stress reduction
*antiOx↑, ALA is being referred as the universal antioxidant
*neuroP↑, ALA has neuroprotective effects on Aβ-mediated cytotoxicity
*Ach↑, ALA show anti-dementia or anti-AD properties by increasing acetylcholine (ACh) production through activation of choline acetyltransferase, which increases glucose absorption
*lipid-P↓, ALA has multiple and complex effects in this way, namely scavenging ROS, transition metal ions, increasing the levels of reduced glutathione [59,63], scavenging of lipid peroxidation products
*IL1β↓, ALA downregulated the levels of the inflammatory cytokines IL-1B and IL-6 in SK-N-BE human neuroblastoma cells
*IL6↓,
TumCP↓, ALA inhibited cell proliferation, [18F]-FDG uptake and lactate formation and increased apoptosis in neuroblastoma cell lines Kelly, SK-N-SH, Neuro-2a and in the breast cancer cell line SkBr3.
FDG↓,
Apoptosis↑,
AMPK↑, ALA suppressed thyroid cancer cell proliferation and growth through activation of AMPK and subsequent down-regulation of mTOR-S6 signaling pathway in BCPAP, HTH-83, CAL-62 and FTC-133 cells lines.
mTOR↓,
EGFR↓, ALA inhibited cell proliferation through Grb2-mediated EGFR down-regulation
TumCI↓, ALA inhibited metastatic breast cancer cells migration and invasion, partly through ERK1/2 and AKT signaling
TumCMig↓,
*memory↑, Alzheimer’s Disease: ALA led to a marked improvement in learning and memory retention
*BioAv↑, Since ALA is poorly soluble, lecithin has been used as an amphiphilic matrix to enhance its bioavailability.
*BioAv↝, ALA were found to be considerably higher in adults with mean age greater than 75 years as compared to young adults between the ages of 18 and 45 years.
*other↓, ALA treatment has been recently studied by some clinical trials to explain its efficacy in preventing miscarriage
*other↝, 1800 mg of ALA or placebo were administrated orally every day, except during the period 2 days before to 4 days after administration of each dose of platinum to avoid potential interference with platinum’s antitumor effects
*Half-Life↓, Data shows a short half-life and bioavailability of about 30% of ALA due to mechanisms involving hepatic degradation, reduced ALA solubility as well as instability in the stomach.
*BioAv↑, ALA bioavailability is greatly reduced after food intake and it has been recommended that ALA should be admitted at least 2 h after eating or if taken before; meal should be taken at least 30 min after ALA administration
*ChAT↑, ALA show anti-dementia or anti-AD properties by increasing acetylcholine (ACh) production through activation of choline acetyltransferase, which increases glucose absorption
*GlucoseCon↑,
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in-vitro, |
HCC, |
HepG2 |
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in-vitro, |
HCC, |
Hep3B |
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P53↑,
EMT↓,
AMPK↑,
cycD1/CCND1↓,
TumCMig↓, only in HCC cells that express wild type p53
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in-vitro, |
Thyroid, |
BCPAP |
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in-vitro, |
Thyroid, |
HTH-83 |
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in-vitro, |
Thyroid, |
CAL-62 |
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in-vitro, |
Thyroid, |
FTC-133 |
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in-vivo, |
NA, |
NA |
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TumCP↓,
AMPK↑,
mTOR↓,
TumCMig↓,
TumCI↓,
EMT↓,
E-cadherin↑,
β-catenin/ZEB1↓,
Vim↓,
Snail↓,
Twist↓,
TGF-β↓,
p‑SMAD2↓,
TumCG↓, mouse model
TumCMig↓,
TGF-β↓,
TumCMig↓,
MMP2↓,
MMP9↓,
ECM/TCF↓,
p‑SMAD2↓,
p‑SMAD3↓,
SMAD4↓,
p‑ERK↓,
ROS↓, reduced (TGF‐β1‐induced) intracellular ROS generation
NOX4↓,
SOD2↑,
SIRT1↑, Andro protects AECs from EMT partially by activating Sirt1/FOXO3‐mediated anti‐oxidative stress pathway
FOXO3↑,
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in-vitro, |
GBM, |
GBM8401 |
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in-vitro, |
GBM, |
U251 |
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TumCI↓,
TumCMig↓,
MMP2↓,
ERK↝, combination of andrographolide and an ERK inhibitor might be a good strategy for preventing GBM metastasis
*BioAv↓, Apigenin is not easily absorbed orally because of its low water solubility, which is only 2.16 g/mL
*Half-Life∅, Apigenin is slowly absorbed and eliminated from the body, as evidenced by its half‐life of 91.8 h in the blood
selectivity↑, selective anticancer effects and effective cell cytotoxic activity while exhibiting negligible toxicity to ordinary cells
*toxicity↓, intentional consumption in higher doses, as the toxicity hazard is low
Wnt/(β-catenin)↓, inhibiting the Wnt/β‐catenin
P53↑,
P21↑,
PI3K↓,
Akt↓,
mTOR↓,
TumCCA↑, G2/M
TumCI↓,
TumCMig↓,
STAT3↓, apigenin can activate p53, which improves catalase and inhibits STAT3,
PKM2↓,
EMT↓, reversing increases in epithelial–mesenchymal transition (EMT)
cl‑PARP↑, apigenin increases the cleavage of poly‐(ADP‐ribose) polymerase (PARP) and rapidly enhances caspase‐3 activity,
Casp3↑,
Bax:Bcl2↑,
VEGF↓, apigenin suppresses VEGF transcription
Hif1a↓, decrease in hypoxia‐inducible factor 1‐alpha (HIF‐1α
Dose∅, effectiveness of apigenin (200 and 300 mg/kg) in treating CC was evaluated by establishing xenografts on Balb/c nude mice.
GLUT1↓, Apigenin has been found to inhibit GLUT1 activity and glucose uptake in human pancreatic cancer cells
GlucoseCon↓,
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in-vitro, |
Lung, |
A549 |
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in-vitro, |
Nor, |
BEAS-2B |
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in-vitro, |
Lung, |
H1975 |
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TumCP↓, AGL significantly reduced proliferation, promoted cell apoptosis, and attenuated the migration and invasion of A549 or H1975 cell
Apoptosis↑,
TumCMig↓,
TumCI↓,
Cyt‑c↑, elevated the levels of cytochrome C and MDA
MDA↑,
GSH↓, but reduced the production of GSH in A549 and H1975 cells.
ROS↑, AGL enhanced the accumulation of ROS
PI3K↓, induces ROS accumulation in lung cancer cells by repressing PI3K/Akt/mTOR pathway
Akt↓,
mTOR↓,
TNF-α↓, Apigenin downregulates the TNFα
IL6↓,
IL1α↓,
P53↑,
Bcl-xL↓,
Bcl-2↓,
BAX↑,
Hif1a↓, Apigenin inhibited HIF-1alpha and vascular endothelial growth factor expression
VEGF↓,
TumCCA↑, Apigenin exposure induces G2/M phase cell cycle arrest, DNA damage, apoptosis and p53 accumulation
DNAdam↑,
Apoptosis↑,
CycB/CCNB1↓,
cycA1/CCNA1↓,
CDK1↓,
PI3K↓,
Akt↓,
mTOR↓,
IKKα↓, , decreases IKKα kinase activity,
ERK↓,
p‑Akt↓,
p‑P70S6K↓,
p‑S6↓,
p‑ERK↓, decreased
the expression of phosphorylated (p)-ERK1/2 proteins, p-AKT and p-mTOR
p‑P90RSK↑,
STAT3↓,
MMP2↓, Apigenin down-regulated Signal transducer and activator of transcription 3target genes MMP-2, MMP-9 and vascular endothelial growth factor
MMP9↓,
TumCP↓, Apigenin significantly suppressed colorectal cancer cell proliferation, migration, invasion and organoid growth through inhibiting the Wnt/β-catenin signaling
TumCMig↓,
TumCI↓,
Wnt/(β-catenin)↓,
TumCP↓, We found that API could inhibit the proliferation of Ishikawa cells at IC50 of 45.55 μM, arrest the cell cycle at G2/M phase, induce apoptosis by inhibiting Bcl-xl and increasing Bax, Bak and Caspases.
TumCCA↑,
Apoptosis↑,
Bcl-2↓,
BAX↑,
Bak↑,
Casp↑,
ER Stress↑, Further, API could induce apoptosis by activating the endoplasmic reticulum (ER) stress pathway by increasing the Ca2+, ATF4, and CHOP.
Ca+2↑, after API treatment for 48 h, the intracellular Ca2+ concentration increased in cells in a dose-dependent manner.
ATF4↑,
CHOP↑,
ROS↑, the level of intracellular ROS increased gradually with the increase of API concentration.
MMP↓, mitochondrial membrane potential of 30 μM, 50 μM, and 70 μM groups decreased by 2.19%, 11.32%, and 14.91%, respectively.
TumCMig↓, API inhibits the migration and invasion of Ishikawa cells and the migration and invasion related gene and protein.
TumCI↓,
eff↑, In our study, API restrained the viability of Ishikawa cells, and the inhibition effect of API on Ishikawa cells was better than that of 5-FU.
P53↑, API induces p53 tumor suppressor proteins at the translational level and the induces p21
P21↑,
Cyt‑c↑, After the mitochondria release the Cyto-c, the Caspase-9 is activated, resulting in increased activity of Caspases
Casp9↑, In our study, the expression levels of Bad, Bax, Cyto-c, Caspase-9 and Caspase-3 proteins were up-regulated,
Casp3↑,
Bcl-xL↓, while the expression level of Bcl-xl was down-regulated
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in-vitro, |
BC, |
MDA-MB-231 |
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TumCMig↓, apigenin presents the most potent anti-migration and anti-invasion properties
TumCI↓,
ITGB4↓, Apigenin inhibits the HGF-induced clustering of beta 4 integrin at actin-rich adhesive site and lamellipodia through PI3K-dependent manner.
TumCP↓, API suppresses 4T1 cells proliferation
TumCMig↓, API restraints 4T1 cells migration and invasion
TumCI↓,
Apoptosis↑, API triggers 4T1 apoptosis and modulates the expression levels of apoptotic-associated proteins in 4T1 cells
MMP↑, API triggers the depolarization of ΔΨm in 4T1 cells
ROS↑, API induces ROS generation
p‑PI3K↓, The results revealed a significant downregulation of p-PI3K/PI3K, p-AKT/AKT, and Nrf2 in 4T1 cells following API treatment
PI3K↓,
Akt↓,
NRF2↓,
AntiTum↑, API exhibits anti-tumor activity in mice
OS↑, results of animal survival experiments show that API can appropriately prolong the survival of mice with mammary gland tumors
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in-vitro, |
CRC, |
SW480 |
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in-vitro, |
CRC, |
HTC15 |
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Wnt/(β-catenin)↓, Apigenin inhibits β‑catenin/TCF/LEF signal activation.
TCF↓,
LEF1↓, LEF
TumCP↓, Apigenin inhibits CRC cell line proliferation
TumCMig↓, Apigenin inhibits migration and invasion of SW480 cells and growth of intestinal organoids.
TumCI↓,
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in-vitro, |
CRC, |
SW480 |
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in-vitro, |
CRC, |
DLD1 |
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NEDD9↓, Inhibition of apigenin on cell migration, invasion, and metastasis through downregulation of NEDD9 in vitro and in vivo
TumCMig↓, Apigenin attenuates NEDD9 expression, resulting in inhibition on cell migration, invasion, and metastasis of those cells.
TumCI↓,
TumCP↓, reported inhibitory effects on cancer cell proliferation, invasion and migration.
TumCI↓,
TumCMig↓,
Apoptosis↑, ART has been reported to induce apoptosis, differentiation and autophagy in colorectal cancer cells by impairing angiogenesis
Diff↑,
TumAuto↑,
angioG↓,
TumCCA↑, inducing cell cycle arrest (11), upregulating ROS levels, regulating signal transduction [for example, activating the AMPK-mTOR-Unc-51-like autophagy activating kinase (ULK1) pathway in human bladder cancer cells]
ROS↑,
AMPK↑,
mTOR↑,
ChemoSen↑, ART has been shown to restore the sensitivity of a number of cancer types to chemotherapeutic drugs by modulating various signaling pathways
Tf↑, ART could upregulate the mRNA levels of transferrin receptor (a positive regulator of ferroptosis), thus inducing apoptosis and ferroptosis in A549 non-small cell lung cancer (NSCLC) cells.
Ferroptosis↑,
Ferritin↓, ferritin degradation, lipid peroxidation and ferroptosis
lipid-P↑,
CDK1↑, Cyclin-dependent kinase 1, 2, 4 and 6
CDK2↑,
CDK4↑,
CDK6↑,
SIRT1↑, Sirt1 levels
COX2↓,
IL1β↓, IL-1? ?
survivin↓, ART can selectively downregulate the expression of survivin and induce the DNA damage response in glial cells to increase cell apoptosis and cell cycle arrest, resulting in increased sensitivity to radiotherapy
DNAdam↑,
RadioS↑,
angioG↓, The anti-malarial agent dihydroartemisinin (DHA) has strong anti-angiogenic activity.
TumCP↓, DHA shows a dose-dependent inhibition of proliferation and migration of in HUVECs.
TumCMig↓,
NF-kB↓, Our data suggested that DHA inhibits angiogenesis largely through repression of the NF-κB pathway.
TumCP↓,
TumCMig↓,
TumCI↓,
MMP17↓,
p‑EGFR↓,
p‑Akt↓,
| - |
vitro+vivo, |
NSCLC, |
A549 |
|
|
|
- |
vitro+vivo, |
NSCLC, |
H1299 |
|
|
|
TumCCA↑, arresting cell cycle in G1
phase.
CSCs↓,
TumCI↓,
TumCMig↓,
TumCG↓,
Wnt/(β-catenin)↓, main pathway
Nanog↓,
SOX2↓,
OCT4↓, oct3/4
N-cadherin↓,
Vim↓,
E-cadherin↑,
| - |
in-vitro, |
Liver, |
HepG2 |
|
|
|
- |
in-vitro, |
Cerv, |
HeLa |
|
|
|
Dose↝, The combination of ART and Res exhibited the strongest anticancer effect at the ratio of 1:2 (ART to Res).
TumCMig↓, combination of the two drugs also markedly reduced the ability of cell migration
Apoptosis↑, Apoptosis analysis showed that combination of ART and Res significantly increased the apoptosis and necrosis rather than use singly
necrosis↑,
ROS↑, ROS levels were elevated by combining ART with Res.
eff↑, the data suggested that the IC50 of the combination of ART and Res is lower than that of each drug used alone.
TumMeta↓, The included studies demonstrated that aspirin suppresses metastatic dissemination across multiple cancer types through coordinated platelet-dependent and tumor-intrinsic mechanisms.
COX1↓, Aspirin consistently inhibited platelet aggregation and COX-1-dependent TXA2 production, disrupting platelet–tumor cell interactions, intravascular metastatic niche formation, and platelet-mediated immune suppression.
TXA2↓,
AntiAg↑, Beyond platelet effects, aspirin suppressed EMT, migration, and invasion through modulation of EMT transcriptional regulators and inflammatory signaling pathways.
EMT↓,
TumCMig↓,
TumCI↓,
AMPK↑, Additional mechanisms included activation of AMPK, inhibition of c-MYC signaling, regulation of redox-responsive pathways and impairment of anoikis resistance.
cMyc↓,
PGE2↓, Importantly, oral aspirin (20 mg/kg/day; human-equivalent ≈ 150 mg/day), administered before tumor cell injection, prevented platelet-induced metastatic enhancement and suppressed TXA2 and PGE2 production.
Dose↑, medium and high doses of aspirin reduced pulmonary metastatic burden by more than 50%, whereas low-dose aspirin was ineffective.
RadioS↑, Wang et al. [45] demonstrated that low-dose aspirin suppresses radiotherapy-induced release of immunosuppressive exosomes in breast cancer, restoring NK-cell proliferation and enhancing antitumor immunity in vivo.
PD-L1↓, Similarly, Xiao et al. [46] showed that aspirin epigenetically downregulates PD-L1 expression by inhibiting KAT5-dependent histone acetylation, thereby restoring T-cell activation
E-cadherin↑, Aspirin restored E-cadherin expression and suppressed EMT regulators, including Slug, vimentin, Twist, MMP-2, and MMP-9.
EMT↓,
Slug↓,
Vim↓,
Twist↓,
MMP2↓,
MMP9↓,
other↑, definitive conclusions regarding clinical efficacy across cancer types cannot yet be drawn. Nevertheless, the consistency of mechanistic signals across experimental systems supports further investigation of aspirin as a low-cost adjunct in oncology
| - |
in-vitro, |
CRC, |
HCT116 |
|
|
|
- |
in-vitro, |
CRC, |
SW48 |
|
|
|
TumCG↓, WA inhibits CRC’s growth, migration, and invasion by inhibiting the HSP90/HIF-1α/EMT axis.
TumCMig↓,
TumCI↓,
HSP90↓,
Hif1a↓,
EMT↓,
| - |
in-vitro, |
HCC, |
HepG2 |
|
|
|
- |
in-vitro, |
HCC, |
Hep3B |
|
|
|
- |
in-vitro, |
HCC, |
HUH7 |
|
|
|
NF-kB↓, We found that many of Nuclear factor kappa B (NF-κB), angiogenesis and inflammation associated proteins secretion is downregulated upon Withaferin A treatment.
angioG↓,
Inflam↓,
TumCP↓, uppressed the proliferation, migration, invasion, and anchorage-independent growth of these HCC cells.
TumCMig↓,
TumCI↓,
Sp1/3/4↓, Withaferin A inhibits NF-κB, Specificity protein 1 (Sp1) transcription factors, and downregulates Vascular Endothelial Growth Factor (VEGF) gene expression
VEGF↓,
angioG↓, Withaferin A (2.5 µM) treatment decreased the secretion of various angiogenesis-related markers, growth factors, and cytokines (Serpin F1(PEDF), uPA, PDGF-AA, Angiogenin, Endothelin-1, Macrophage migration inhibitory factor (MIF), PAI-1, MCP1, ICAM-1
uPA↓,
PDGF↓,
MCP1↓,
ICAM-1↓,
*NRF2↑, It also upregulates the Nuclear factor erythroid 2-related factor 2 (Nrf2) transcription factor and protects from Acetaminophen-induced hepatotoxicity and liver injury
*hepatoP↑,
| - |
in-vitro, |
PC, |
PANC1 |
|
|
|
- |
in-vitro, |
PC, |
Hs766t |
|
|
|
ChemoSen↑, combination treatment being the most effective
ROS↑, which were attenuated by N-acetylcysteine
Apoptosis↑,
TumCMig↓, strongest inhibition was observed when both compounds were co-administered
F-actin↓, leading to F-actin depolymerization
YMcells↓, greater reduction in cell stiffness compared to individual treatments
NF-kB↓, relative luciferase activity, which reflects NF-κB activity, was markedly elevated following treatment with GC (Figure 7). In contrast, treatment with WFA resulted in a notable decline in luciferase activity, particularly when combined with GC.
| - |
in-vitro, |
Lung, |
A549 |
|
|
|
- |
in-vitro, |
Lung, |
H1299 |
|
|
|
TumCMig↓,
TumCI↓,
EMT↓,
p‑SMAD2↓,
p‑SMAD3↓,
p‑NF-kB↓,
| - |
in-vitro, |
CRC, |
HCT116 |
|
|
|
- |
in-vivo, |
NA, |
NA |
|
|
|
TumCP↓,
TumCMig↓,
STAT3↓, implicated in the development and progression of colon cancer.
TumVol↓,
TumW↓,
| - |
in-vitro, |
EC, |
K1 |
|
|
|
- |
in-vitro, |
Nor, |
THESCs |
|
|
|
TumCP↓,
*toxicity↓, comparatively lower toxicity against the THESCs normal cells
Apoptosis↑,
TumCCA↑, G2/M cell cycle arrest
TumCMig↓, 53%
TumCI↓, 40%
p‑SMAD2↓,
TGF-β↓,
*toxicity↓, Cytotoxicity of withaferin A was comparatively lower against normal THESCs endometrial cells (IC50 value of 76 µM) when compared to cancerous KLE cells.
Akt↓, WA, a natural compound, resulted in significant inhibition of AKT activity and led to the inhibition of cell proliferation, migration and invasion
TumCP↓,
TumCMig↓,
TumCI↓,
EMT↓, by downregulating the epithelial to mesenchymal transition (EMT) markers in CRC cells overexpressing AKT
Snail↓, Further, significant inhibition of some important EMT markers, i.e., Snail, Slug, β-catenin and vimentin, was observed in WA-treated human CRC cells overexpressing AKT
Slug↓,
β-catenin/ZEB1↓,
Vim↓,
angioG↓, Significant inhibition of micro-vessel formation and the length of vessels were evident in WA-treated tumors, which correlated with a low expression of the angiogenic marker RETIC
| - |
vitro+vivo, |
Melanoma, |
A375 |
|
|
|
- |
vitro+vivo, |
Melanoma, |
A2058 |
|
|
|
ROS↓, Astaxanthin reduces melanoma ROS in a dose-dependent manner.
MMPs↓, Astaxanthin inhibits cellular MMPs to suppress migration and metastasis.
TumCMig↓,
TumMeta↓,
TumCCA↑, Astaxanthin induces sub-G1 arrest to trigger apoptosis in vitro and in vivo.
antiOx↑, Because astaxanthin is a potent scavenger of free radicals and quencher of reactive oxygen and nitrogen species, its antioxidant effects are even stronger than those of carotene carotenoids
MMP1↓, Astaxanthin treatment inhibited expressions of MMP-1, -2 and -9 in a dose-dependent manner.
MMP2↓,
MMP9↓,
| - |
in-vitro, |
BC, |
MDA-MB-231 |
|
|
|
- |
in-vitro, |
Nor, |
MCF10 |
|
|
|
TumCP↓, application of ASX significantly reduced proliferation rates and inhibited breast cancer cell migration compared to control normal breast epithelial cells.
TumCMig↓,
selectivity↑,
*BDNF↑, ASX increases brain derived neurotropic factor (BDNF) protein levels, while concurrently decreasing oxidative stress levels [6]
*ROS↓,
*TNF-α↓, ASX decreases the amount of inflammatory markers such as TNF-α, IL-6, and IFN-γ via NFκβ inhibition [7].
*IL6↓,
*IFN-γ↓,
*NF-kB↓,
BAX⇅, In the triple-negative cell line MDA-MB-231 both BAX and BCL-2 mRNA levels were reduced following ASX treatments. while BAX levels were elevated following treatment with 50 μM ASX.
Bcl-2↓,
*antiOx↑, ASX is a marine-based ketocarotenoid that has potent antioxidant characteristics
radioP↑, Incorporation of ASX into anticancer therapy will help control tumor growth and potentially reduce the impact of radiation therapy and chemotherapy associated side effects.
ChemoSen↑,
| - |
in-vitro, |
Pca, |
DU145 |
|
|
|
- |
in-vivo, |
NA, |
NA |
|
|
|
TumCP↓, Astaxanthin resulted in suppression of the proliferation of DU145 cells and the level of STAT3.
STAT3↓, Thus, astaxanthin inhibits the proliferation of DU145 cells by reducing the expression of STAT3.
Apoptosis↑, treatment of DU145 cells with astaxanthin decreased the cloning ability, increased the apoptosis percentage and weakened the abilities of migration and invasion of the cells.
TumCMig↓,
TumCI↓,
*antiOx↑, Reports indicate that ASX’s antioxidant efficacy surpasses that of vitamin C, vitamin E, coenzyme Q10, and alpha-lipoic acid.
*neuroP↑, Astaxanthin is a powerful antioxidant compound that supports heart, skin, and eye health, helps manage diabetes, and offers brain-protective benefits.
AntiCan↑, Astaxanthin shows promise as an anticancer agent by limiting tumor growth, inducing cancer cell death, and reducing the spread of malignant cells.
TumCG↓,
TumCD↑,
TumCMig↓,
ChemoSen↑, Astaxanthin enhances the effects of chemotherapy, reduces its side effects, and helps overcome drug resistance.
chemoP↑,
*BioAv↓, Astaxanthin has limited absorption in the body, but using nanocarriers like nanoparticles and nano-emulsions can greatly enhance its bioavailability and therapeutic potential.
TumCP↓, ASX inhibits tumor formation, primarily by hindering cell proliferation, inducing cell cycle arrest, and promoting apoptosis.
TumCCA↑,
Apoptosis↑,
BioAv↑, Nanotechnology: a solution for improving astaxanthin bioavailability
| - |
in-vitro, |
Pca, |
LNCaP |
|
|
|
- |
in-vitro, |
Pca, |
MCF-7 |
|
|
|
Bax:Bcl2↑, combination treatment significantly increased the ratio of Bax to Bcl-2 proteins, decreased the activation of NFκB, PI3K/Akt and Stat3
NF-kB↓, arctigenin demonstrated the strongest ability to inhibit the activation of both PI3K/Akt and NFκB pathways in both LNCaP and MCF-7 cells.
PI3K/Akt↓,
STAT3↓,
chemoPv↑, combining Arc and EGCG with Cur to enhance chemoprevention in both prostate and breast cancer.
TumCP↓, combining Arc and EGCG with Cur to enhance chemoprevention in both prostate and breast cancer.
TumCCA↑, EGCG significantly increased the effect of curcumin on cell cycle arrest at G0/G1 phase in MCF-7 cells, and the effect was further enhanced by the addition of arctigenin
TumCMig↓, EGCG and arctigenin alone or in combination with curcumin significantly decreased the number of migrated MCF-7 cells compared to control
HMG-CoA↓, atorvastatin as a reductase (HMG-CoA) inhibitor might affect proliferation, migration, and survival of cancer cells.
TumCP↓,
TumCMig↓,
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
| - |
in-vitro, |
Nor, |
MCF10 |
|
|
|
- |
in-vivo, |
NA, |
NA |
|
|
|
*TumCMig↓,
*F-actin↓,
*E-cadherin↑,
*ZO-1↑,
*N-cadherin↓,
*Vim↓,
*Snail↓,
*cal2↓, baicalein inhibited calpain-2 by decreasing intracellular calcium ion levels
*Ca+2↝, Effects of baicalein on fibronectin (FN)-induced intracellular elevation of Ca2+
Returns elevated levels close to back to original levels.
Showing Research Papers: 1 to 50 of 361
Page 1 of 8
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 361
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, Ferroptosis↑, 1, GSH↓, 3, lipid-P↑, 1, MDA↑, 1, NOX4↓, 1, NRF2↓, 1, ROS↓, 2, ROS↑, 14, SOD2↑, 1, TrxR↓, 1,
Metal & Cofactor Biology ⓘ
Ferritin↓, 1, Tf↑, 1,
Mitochondria & Bioenergetics ⓘ
ATP↓, 1, MMP↓, 2, MMP↑, 1,
Core Metabolism/Glycolysis ⓘ
AMPK↑, 6, cMyc↓, 1, FDG↓, 1, GlucoseCon↓, 1, HMG-CoA↓, 1, PDH↑, 1, PI3K/Akt↓, 1, PKM2↓, 1, p‑S6↓, 1, SIRT1↑, 2,
Cell Death ⓘ
Akt↓, 9, p‑Akt↓, 2, Apoptosis↑, 16, Bak↑, 1, BAX↑, 3, BAX⇅, 1, Bax:Bcl2↑, 2, Bcl-2↓, 6, Bcl-xL↓, 2, Casp↑, 2, Casp12↑, 1, Casp3↑, 4, cl‑Casp3↑, 1, Casp8↑, 1, Casp9↑, 3, cl‑Casp9↑, 1, Cyt‑c↑, 3, Fas↓, 1, Fas↑, 1, FasL↓, 1, Ferroptosis↑, 1, JNK↓, 1, JNK↑, 1, necrosis↑, 1, p38↑, 1, survivin↓, 1, TumCD↑, 3,
Kinase & Signal Transduction ⓘ
Sp1/3/4↓, 1,
Transcription & Epigenetics ⓘ
other↓, 1, other↑, 1, other↝, 1, tumCV↓, 2, YMcells↓, 1,
Protein Folding & ER Stress ⓘ
CHOP↑, 1, ER Stress↑, 2, HSP90↓, 1,
Autophagy & Lysosomes ⓘ
TumAuto↑, 1,
DNA Damage & Repair ⓘ
CHK1↓, 1, DNAdam↑, 3, P53↑, 7, cl‑PARP↑, 2, PCNA↓, 1,
Cell Cycle & Senescence ⓘ
CDK1↓, 2, CDK1↑, 1, CDK2↑, 1, CDK4↑, 1, cycA1/CCNA1↓, 1, CycB/CCNB1↓, 3, cycD1/CCND1↓, 1, P21↑, 3, TumCCA↑, 13,
Proliferation, Differentiation & Cell State ⓘ
CSCs↓, 1, Diff↑, 1, EMT↓, 11, ERK↓, 3, ERK↝, 1, p‑ERK↓, 2, FOXO3↑, 1, GSK‐3β↓, 1, mTOR↓, 5, mTOR↑, 1, mTORC2↓, 1, Nanog↓, 1, NOTCH1↓, 1, OCT4↓, 1, p‑P70S6K↓, 1, p‑P90RSK↑, 1, PI3K↓, 5, p‑PI3K↓, 1, SOX2↓, 1, STAT3↓, 6, TCF↓, 1, TumCG↓, 7, Wnt↓, 1, Wnt/(β-catenin)↓, 4,
Migration ⓘ
AntiAg↑, 1, Ca+2↑, 2, E-cadherin↑, 6, F-actin↓, 1, p‑FAK↓, 1, ITGB1↓, 1, ITGB4↓, 1, Ki-67↓, 1, LEF1↓, 1, MMP1↓, 1, MMP17↓, 1, MMP2↓, 8, MMP9↓, 6, MMPs↓, 1, N-cadherin↓, 3, NEDD9↓, 1, PDGF↓, 1, PKCδ↓, 1, Slug↓, 2, p‑SMAD2↓, 4, p‑SMAD3↓, 2, SMAD4↓, 1, Snail↓, 3, TGF-β↓, 3, TGF-β1↓, 1, TumCI↓, 29, TumCMig↓, 49, TumCP↓, 25, TumMeta↓, 3, Twist↓, 2, uPA↓, 1, VCAM-1↓, 1, Vim↓, 6, Vim↑, 1, β-catenin/ZEB1↓, 3,
Angiogenesis & Vasculature ⓘ
angioG↓, 5, ATF4↑, 1, ECM/TCF↓, 1, EGFR↓, 1, p‑EGFR↓, 1, EGR4↓, 1, Hif1a↓, 4, Hif1a↑, 1, TXA2↓, 1, VEGF↓, 4, VEGFR2↓, 1,
Barriers & Transport ⓘ
GLUT1↓, 1,
Immune & Inflammatory Signaling ⓘ
COX1↓, 1, COX2↓, 1, ICAM-1↓, 1, IKKα↓, 1, IL1α↓, 1, IL1β↓, 1, IL6↓, 2, IL8↓, 1, Inflam↓, 2, MCP1↓, 1, NF-kB↓, 6, p‑NF-kB↓, 1, p‑NF-kB↑, 1, PD-L1↓, 1, PGE2↓, 1, TNF-α↓, 2,
Hormonal & Nuclear Receptors ⓘ
CDK6↑, 1,
Drug Metabolism & Resistance ⓘ
BioAv↑, 1, BioAv↝, 1, ChemoSen↑, 5, Dose↑, 1, Dose↝, 2, Dose∅, 1, eff↑, 3, eff↝, 2, Half-Life↓, 1, RadioS↑, 2, selectivity↑, 5,
Clinical Biomarkers ⓘ
EGFR↓, 1, p‑EGFR↓, 1, Ferritin↓, 1, IL6↓, 2, Ki-67↓, 1, PD-L1↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 4, AntiTum↑, 2, chemoP↑, 3, chemoPv↑, 1, OS↑, 1, radioP↑, 1, TumVol↓, 1, TumW↓, 1,
Total Targets: 190
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 6, GSH↑, 2, GSTs↑, 1, Keap1↓, 1, lipid-P↓, 2, MDA↓, 1, MPO↓, 1, NRF2↑, 2, ROS↓, 4, SOD↑, 1, TBARS↓, 1,
Metal & Cofactor Biology ⓘ
IronCh↑, 1,
Core Metabolism/Glycolysis ⓘ
ALAT↓, 1, GlucoseCon↑, 1, H2S↑, 1, LDH↓, 2,
Cell Death ⓘ
Akt↓, 1, iNOS↓, 1,
Transcription & Epigenetics ⓘ
Ach↑, 1, other↓, 1, other↑, 1, other↝, 1,
Proliferation, Differentiation & Cell State ⓘ
PI3K↓, 1,
Migration ⓘ
Ca+2↝, 1, cal2↓, 1, E-cadherin↑, 1, F-actin↓, 1, N-cadherin↓, 1, Snail↓, 1, TumCMig↓, 1, Vim↓, 1, ZO-1↑, 1,
Angiogenesis & Vasculature ⓘ
NO↓, 1,
Barriers & Transport ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IFN-γ↓, 1, IL1β↓, 1, IL6↓, 3, Imm↑, 1, Inflam↓, 2, NF-kB↓, 2, PGE2↓, 1, TNF-α↓, 2,
Synaptic & Neurotransmission ⓘ
BDNF↑, 1, ChAT↑, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 2, BioAv↑, 2, BioAv↝, 1, eff↑, 1, Half-Life↓, 1, Half-Life↝, 1, Half-Life∅, 1,
Clinical Biomarkers ⓘ
ALAT↓, 1, AST↓, 1, BP↓, 1, creat↓, 1, GutMicro↑, 1, IL6↓, 3, LDH↓, 2,
Functional Outcomes ⓘ
cardioP↑, 1, cognitive↑, 1, hepatoP↑, 2, memory↑, 2, neuroP↑, 4, toxicity↓, 4,
Infection & Microbiome ⓘ
Bacteria↓, 1,
Total Targets: 66
Scientific Paper Hit Count for: TumCMig, Tumor cell migration
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#:326 State#:% Dir#:1
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