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.
Scientific Papers found: Click to Expand⟱
5204- CAP,    Low-concentration capsaicin promotes colorectal cancer metastasis by triggering ROS production and modulating Akt/mTOR and STAT-3 pathways
- in-vitro, Colon, SW480 - in-vitro, Colon, CT26
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↑,

1518- CAP,    Capsaicin-mediated tNOX (ENOX2) up-regulation enhances cell proliferation and migration in vitro and in vivo
- in-vitro, CRC, HCT116
ENOX2↑, low concentrations s (<10uM) of capsaicin up-regulates tNOX
TumCP↑,
TumCMig↑,
Dose?, <10uM
eff↑, tNOX knockdown reverses capsaicin-induced cell migration and growth

6182- Cu,    Role of cuproptosis in digestive system tumors (Review)
- Review, Var, NA
Cupro↑, As copper dysregulation is common in cancer cells, targeting copper levels or metabolic pathways can trigger cuproptosis, thereby inhibiting tumor growth and progression.
TumCG↓,
Apoptosis↑, Copper can trigger multiple forms of cell death, including apoptosis, oxidative stress-induced necrosis, autophagy and ferroptosis
ROS↑,
Ferroptosis↑,
ETC↓, . Their disruption impairs the electron transport chain and decreases ATP synthesis and mitochondrial membrane potential (76).
MMP↓,
Ca+2↑, Consequently, mitochondrial energy production decreases, accompanied by increased inner membrane permeability, elevated Ca2+ concentration and the accumulation of ROS (77).
Fenton↑, Cu2+ catalyzes the Fenton-like reaction, generating hydroxyl radicals that initiate oxidative stress, leading to extensive cell damage and death (96)
lipid-P↑, These radicals also induce lipid peroxidation, compromising the integrity and fluidity of cell membranes and increasing membrane permeability (99).
MPT↑,
ATP↓, Excess ROS decrease the mitochondrial membrane potential and ATP synthesis and promote cytochrome c release, ultimately activating caspase cascades and triggering apoptosis
Cyt‑c↑,
Casp↑,
angioG↑, Mechanistically, copper promotes tumor progression through multiple pathways. First, copper stimulates angiogenesis by activating angiogenic factors and enhancing the proliferation and migration of vascular endothelial cells
TumCP↑,
TumCMig↑,
TumCI↑, Second, copper serves as a cofactor for several metalloenzymes, including MMP-9, SOD1, vascular adhesion protein-1 and lysyl oxidase (LOX), all of which are key for cancer invasion and metastasis
TumMeta↑,
DDS↑, tussah silk fibroin (TSF)-based nanoparticles (NPs) use TME-responsive release mechanisms to deliver copper and the cuproptosis-inducing drug ES directly to pancreatic cancer cells.
eff↑, suppressed by the copper chelator TTM, further confirming the mechanism of copper-induced cell death. Furthermore, 2-deoxy-D-glucose, a glycolysis inhibitor, can significantly enhance cuproptosis

1654- FA,    Molecular mechanism of ferulic acid and its derivatives in tumor progression
- Review, Var, NA
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

4515- MAG,    Magnolol as a Potential Anticancer Agent: A Proposed Mechanistic Insight
- Review, Var, NA
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

2249- MF,    Pulsed electromagnetic fields modulate energy metabolism during wound healing process: an in vitro model study
- in-vitro, Nor, L929
*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↑,

1132- RT,    Rutin Promotes Proliferation and Orchestrates Epithelial–Mesenchymal Transition and Angiogenesis in MCF-7 and MDA-MB-231 Breast Cancer Cells
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7
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)

1222- Z,    Zinc regulates primary ovarian tumor growth and metastasis through the epithelial to mesenchymal transition
- in-vitro, Ovarian, NA
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 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ENOX2↑, 1,   Fenton↑, 1,   Ferroptosis↑, 1,   GSH↓, 1,   lipid-P↑, 1,   PYCR1↓, 1,   ROS↑, 3,   SOD↓, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   ETC↓, 1,   FGFR1↓, 1,   MMP↓, 1,   MPT↑, 1,  

Core Metabolism/Glycolysis ⓘ

CAIX↓, 1,   cMyc↓, 1,   Glycolysis↓, 1,   LDH↓, 1,   PKM2↓, 1,  

Cell Death ⓘ

Akt↓, 2,   Akt↑, 1,   Apoptosis↑, 3,   BAX↑, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 1,   Casp↑, 1,   Casp3↑, 1,   Cupro↑, 1,   Cyt‑c↑, 1,   Ferroptosis↑, 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,   TumCG↓, 1,  

Migration ⓘ

Ca+2↑, 1,   E-cadherin↓, 1,   Ki-67↓, 1,   MMP2↓, 1,   MMP9↑, 1,   N-cadherin↑, 1,   TumCI↓, 1,   TumCI↑, 3,   TumCMig↑, 7,   TumCP↓, 2,   TumCP↑, 3,   TumMeta↑, 2,   Vim↑, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   angioG↑, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   JAK2↓, 1,   NF-kB↓, 2,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   DDS↑, 1,   Dose?, 1,   eff↑, 3,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

Ki-67↓, 1,   LDH↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   ChemoSideEff↓, 1,   MKI67↑, 1,   TumW↓, 1,  
Total Targets: 78

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
2 Capsaicin
1 Copper and Cu NanoParticles
1 Ferulic acid
1 Magnolol
1 Magnetic Fields
1 Rutin
1 Zinc
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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