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⟱
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in-vitro, |
Colon, |
SW480 |
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in-vitro, |
Colon, |
CT26 |
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TumCP↓, high-concentration of capsaicin (≥ 200 µM for SW480 and CT-26 cell lines; ≥ 25 µM for HCT116 cell line) inhibited CRC cell proliferation in a dose-dependent manner
TumCMig↑, low-concentration of capsaicin (100 µM for SW480 and CT-26 cell lines; 12.5 µM for HCT116 cell line) enhanced both migratory and invasive capability of these cells
TumCI↑,
EMT↑, 100 µM capsaicin induced epithelial-to-mesenchymal (EMT), up-regulated expression of MMP-2 and MMP-9, and activated Akt/mTOR and STAT-3 pathways in SW480 cells.
MMP2↓,
MMP9↑,
STAT3↑,
TumMeta↑, capsaicin-induced metastasis of CRC cells was mediated by modulating reactive oxygen species (ROS) production.
ROS↑,
ENOX2↑, low concentrations s (<10uM) of capsaicin up-regulates tNOX
TumCP↑,
TumCMig↑,
Dose?, <10uM
eff↑, tNOX knockdown reverses capsaicin-induced cell migration and growth
AntiCan↑, FA has anti-inflammatory, analgesic, anti-radiation, and immune-enhancing effects and also shows anticancer activity,
Inflam↓,
RadioS↑,
ROS↑, FA can cause mitochondrial apoptosis by inducing the generation of intracellular reactive oxygen species (ROS)
Apoptosis↑,
TumCCA↑, G0/G1 phase
TumCMig↑, inducing autophagy; inhibiting cell migration, invasion, and angiogenesis
TumCI↓,
angioG↓,
ChemoSen↑, synergistically improving the efficacy of chemotherapy drugs and reducing adverse reactions.
ChemoSideEff↓,
P53↑, FA could increase the expression level of p53 in MIA PaCa-2 pancreatic cancer cells
cycD1/CCND1↓, while reducing the expression levels of cyclin D1 and cyclin-dependent kinase (CDK) 4/6.
CDK4↓,
CDK6↓,
TumW↓, FA treatment was found to reduce tumor weight in a dose-dependent manner, increase miR-34a expression, downregulate Bcl-2 protein expression, and upregulate caspase-3 protein expression
miR-34a↑,
Bcl-2↓,
Casp3↑,
BAX↑,
β-catenin/ZEB1↓, isoferulic acid dose-dependently downregulated the expression of β-catenin and MYC proto-oncogene (c-Myc), inducing apoptosis
cMyc↓,
Bax:Bcl2↑, FXS-3 can inhibit the activity of A549 cells by upregulating the Bax/Bcl-2 ratio
SOD↓, After treatment with FA, Cao et al. [40] observed an increase in ROS production and a decrease in superoxide dismutase activity and glutathione content in EC-1 and TE-4 oesophageal cancer cells
GSH↓,
LDH↓, FA could promote the release of lactate dehydrogenase (LDH)
ERK↑, A can activate the ERK1/2 pathway
eff↑, conjugated zinc oxide nanoparticles with FA (ZnONPs-FA) to act on hepatoma Huh-7 and HepG2 cells. The results showed that ZnONPs-FA could induce oxidative DNA damage and apoptosis by inducing ROS production.
JAK2↓, by inhibiting the JAK2/STAT6 immune signaling pathway
STAT6↓,
NF-kB↓, thus inhibiting the activation of NF-κB
PYCR1↓, FA can target PYCR1 and inhibit its enzyme activity in a concentration-dependent manner.
PI3K↓, FA inhibits the activation of the PI3K/AKT pathway
Akt↓,
mTOR↓, FA could significantly reduce the expression level of mTOR mRNA and Ki-67 protein in A549 lung cancer graft tissue
Ki-67↓,
VEGF↓,
FGFR1↓, FA is a novel FGFR1 inhibitor
EMT↓, FA can inhibit EMT
CAIX↓, selectively inhibit CAIX
LC3II↑, Autophagy vacuoles and increased LC3-II and p62 autophagy proteins were observed after treatment with this compound
p62↑,
PKM2↓, FA could inhibit the expression of PKM2 and block aerobic glycolysis
Glycolysis↓,
*BioAv↓, FA has poor solubility in water and a poor ability to pass through biological barriers [118]; therefore, the extent to which it is metabolized in vivo after oral administration is largely unknown
AntiCan↑, Magnolol exerted anticancer effects through inhibiting proliferation, inducing cell cycle arrest, provoking apoptosis, restraining migration and invasion, and suppressing angiogenesis.
TumCP↓,
TumCCA↑, Magnolol Induces Cell Cycle Arrest
Apoptosis↑,
TumCMig↑,
angioG↓,
PI3K↓, Magnolol Inhibits PI3K/Akt/mTOR Signaling
Akt↓,
mTOR↓,
MAPK↓, Magnolol Inhibits MAPK Signaling
NF-kB↓, Magnolol Inhibits NF-κB Signaling
*TumCMig↑, PEMFs with specific parameter (4mT, 80 Hz) promoted cell migration and viability.
*tumCV↑,
*Glycolysis↑, PEMFs-exposed L929 cells was highly glycolytic for energy generation
*ROS↓, PEMFs enhanced intracellular acidification and maintained low level of intracellular ROS in L929 cells.
*mitResp↓, shifting from mitochondrial respiration to glycolysis
*other↝, Furthermore, the analysis of ECAR/ OCR basal ratio demonstrated a tendency toward to glycolytic phenotype in L929 cells under PEMF exposure, compared to control group
*OXPHOS↓, PEMFs promoted the transformation of energy metabolism pattern from oxidative phosphorylation to aerobic glycolysis
*pH↑, result of pH detection by flow cytometer indicated the pH level in L929 cells was significantly increased in the PEMFs group compared to the control group
*antiOx↑, PEMFs upregulated the expression of antioxidant or glycolysis related genes
*PFKM↑, Pfkm, Pfkl, Pfkp, Pkm2, Hk2, Glut1, were also significantly up-regulated in the PEMFs group
*PFKL↑,
*PKM2↑,
*HK2↑,
*GLUT1↑,
*GPx1↑, GPX1, GPX4 and Sod 1 expression were significantly higher in the PEMFs group compared to the control group
*GPx4↑,
*SOD1↑,
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in-vitro, |
BC, |
MDA-MB-231 |
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in-vitro, |
BC, |
MCF-7 |
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Vim↑,
N-cadherin↑, CDH2
E-cadherin↓,
TumCP↑,
TumCMig↑,
tumCV↑, increased the number of viable cells at concentrations more than 200 µM.
MKI67↑, rutin (200 μM)
EMT↑, zinc contributes to ovarian tumor metastasis by promoting EMT through a MTF-1 dependent pathway
TumCMig↑,
TumCI↑,
ERK↑,
Akt↑, .
Showing Research Papers: 1 to 7 of 7
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
ENOX2↑, 1, GSH↓, 1, PYCR1↓, 1, ROS↑, 2, SOD↓, 1,
Mitochondria & Bioenergetics ⓘ
FGFR1↓, 1,
Core Metabolism/Glycolysis ⓘ
CAIX↓, 1, cMyc↓, 1, Glycolysis↓, 1, LDH↓, 1, PKM2↓, 1,
Cell Death ⓘ
Akt↓, 2, Akt↑, 1, Apoptosis↑, 2, BAX↑, 1, Bax:Bcl2↑, 1, Bcl-2↓, 1, Casp3↑, 1, MAPK↓, 1,
Transcription & Epigenetics ⓘ
tumCV↑, 1,
Autophagy & Lysosomes ⓘ
LC3II↑, 1, p62↑, 1,
DNA Damage & Repair ⓘ
P53↑, 1,
Cell Cycle & Senescence ⓘ
CDK4↓, 1, cycD1/CCND1↓, 1, TumCCA↑, 2,
Proliferation, Differentiation & Cell State ⓘ
EMT↓, 1, EMT↑, 2, ERK↑, 2, miR-34a↑, 1, mTOR↓, 2, PI3K↓, 2, STAT3↑, 1, STAT6↓, 1,
Migration ⓘ
E-cadherin↓, 1, Ki-67↓, 1, MMP2↓, 1, MMP9↑, 1, N-cadherin↑, 1, TumCI↓, 1, TumCI↑, 2, TumCMig↑, 6, TumCP↓, 2, TumCP↑, 2, TumMeta↑, 1, Vim↑, 1, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 2, VEGF↓, 1,
Immune & Inflammatory Signaling ⓘ
Inflam↓, 1, JAK2↓, 1, NF-kB↓, 2,
Hormonal & Nuclear Receptors ⓘ
CDK6↓, 1,
Drug Metabolism & Resistance ⓘ
ChemoSen↑, 1, Dose?, 1, eff↑, 2, RadioS↑, 1,
Clinical Biomarkers ⓘ
Ki-67↓, 1, LDH↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 2, ChemoSideEff↓, 1, MKI67↑, 1, TumW↓, 1,
Total Targets: 63
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, GPx1↑, 1, GPx4↑, 1, OXPHOS↓, 1, ROS↓, 1, SOD1↑, 1,
Mitochondria & Bioenergetics ⓘ
mitResp↓, 1,
Core Metabolism/Glycolysis ⓘ
Glycolysis↑, 1, HK2↑, 1, PFKL↑, 1, PFKM↑, 1, PKM2↑, 1,
Transcription & Epigenetics ⓘ
other↝, 1, tumCV↑, 1,
Migration ⓘ
TumCMig↑, 1,
Barriers & Transport ⓘ
GLUT1↑, 1,
Cellular Microenvironment ⓘ
pH↑, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1,
Total Targets: 18
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
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