TumMeta Cancer Research Results

TumMeta, Cancer Metastasis: Click to Expand ⟱
Source:
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Cancer metastasis is the process by which cancer cells spread from the original (primary) tumor to other parts of the body, forming new (secondary) tumors. This occurs when cancer cells invade surrounding tissues, enter the bloodstream or lymphatic system, and travel to distant organs or tissues.


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↑,

2786- CHr,    Chemopreventive and therapeutic potential of chrysin in cancer: mechanistic perspectives
- Review, Var, NA
Apoptosis↑, chrysin inhibits cancer growth through induction of apoptosis, alteration of cell cycle and inhibition of angiogenesis, invasion and metastasis without causing any toxicity and undesirable side effects to normal cells
TumCCA↑,
angioG↓,
TumCI↓,
TumMeta↑,
*toxicity↓,
selectivity↑,
chemoPv↑, Induction of phase II detoxification enzymes, such as glutathione S-transferase (GST) or NAD(P)H:quinone oxidoreductase (QR) is one of the major mechanism of protection against initiation of carcinogenesis
*GSTs↑,
*NADPH↑,
*GSH↑, upregulation of antioxidant and carcinogen detoxification enzymes (glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR), GST and QR)
HDAC8↓, inhibits of HDAC8 enzymatic activity
Hif1a↓, Prostate DU145: Inhibits HIF-1a expression through Akt signaling and abrogation of VEGF expression
*ROS↓, chrysin (20 and 40 mg/kg) was shown to exhibit chemopreventive activity by ameliorating oxidative stress and inflammation via NF-kB pathway
*NF-kB↓,
SCF↓, Chrysin has also been reported to have the ability to abolish the stem cell factor (SCF)/c-Kit signaling in human myeloid leukemia cells by preventing the PI3 K pathway
cl‑PARP↑, (PARP) and caspase-3 and concurrently decreasing pro-survival proteins survivin and XIAP
survivin↓,
XIAP↓,
Casp3↑, activation of caspase-3 and -9.
Casp9↑,
GSH↓, chrysin sustains a significant depletion of intracellular GSH concentrations in human NSCLC cells
ChemoSen↑, chrysin potentiates cisplatin toxicity, in part, via synergizing pro-oxidant effects of cisplatin by inducing mitochondrial dysfunction, and by depleting cellular GSH, an important antioxidant defense
Fenton↑, ability to participate in a fenton type chemical reaction
P21↑, upregulation of p21 independent of p53 status and decrease in cyclin D1, CDK2 protein levels
P53↑,
cycD1/CCND1↓,
CDK2↓,
STAT3↓, chrysin inhibits angiogenesis through inhibition of STAT3 and VEGF release mediated by hypoxia through Akt signaling pathway
VEGF↓,
Akt↓,
NRF2↓, Chrysin treatment significantly reduced nrf2 expression in cells at both the mRNA and protein levels through down-regulation of PI3K-Akt and ERK pathways.

4826- CUR,    The Bright Side of Curcumin: A Narrative Review of Its Therapeutic Potential in Cancer Management
- Review, Var, NA
*antiOx↑, Curcumin demonstrates strong antioxidant and anti-inflammatory properties, contributing to its ability to neutralize free radicals and inhibit inflammatory mediators
*Inflam↑,
*ROS↓,
Apoptosis↑, Its anticancer effects are mediated by inducing apoptosis, inhibiting cell proliferation, and interfering with tumor growth pathways in various colon, pancreatic, and breast cancers
TumCP↓,
BioAv↓, application is limited by its poor bioavailability due to its rapid metabolism and low absorption.
Half-Life↓,
eff↑, curcumin-loaded hydrogels and nanoparticles, have shown promise in improving curcumin bioavailability and therapeutic efficacy.
TumCCA↑, Studies have demonstrated that curcumin can suppress the proliferation of cancer cells by interfering with the cell cycle [21,22]
BAX↑, Curcumin enhances the expression of pro-apoptotic proteins such as Bax, Bak, PUMA, Bim, and Noxa and death receptors such as TRAIL-R1/DR4 and TRAIL-R2/DR5
Bak↑,
PUMA↑,
BIM↑,
NOXA↑,
TRAIL↑,
Bcl-2↓, curcumin decreases the levels of anti-apoptotic proteins like Bcl-2, Bcl-XL, survin, and XIAP
Bcl-xL↓,
survivin↓,
XIAP↓,
cMyc↓, This shift in the balance of apoptotic regulators facilitates the release of cytochrome c from mitochondria [33,35] and activates caspases
Casp↑,
NF-kB↓, Curcumin suppresses the activity of key transcription factors like NF-κB, STAT3, and AP-1 and interferes with critical signal transduction pathways such as PI3K/Akt/mTOR and MAPK/ERK.
STAT3↓,
AP-1↓,
angioG↓, curcumin inhibits angiogenesis and metastasis by downregulating VEGF, VEGFR2, and matrix metalloproteinases (MMPs).
TumMeta↑,
VEGF↓,
MMPs↓,
DNMTs↓, Epigenetic modifications through the inhibition of DNA methyltransferases (DNMTs) and histone deacetylases (HDACs) further contribute to its anticancer properties.
HDAC↓,
ROS↑, curcumin-loaded nanoparticles showed significant cytotoxicity in the SCC25, MDA-MB-231, and A549 cell lines, with a decrease in tumor cell proliferation, an increase in ROS, and an increase in apoptosis.

1190- Gb,    Extract of Ginkgo biloba exacerbates liver metastasis in a mouse colon cancer Xenograft model
- in-vivo, CRC, SW-620
TumMeta↑, EGb significantly increased the rate of metastasis in mouse liver
Ki-67↑, EGb significantly increased the percentage of Ki67-positive cells in liver tumors when compared to tumors from PBS controls

3277- Lyco,    Recent trends and advances in the epidemiology, synergism, and delivery system of lycopene as an anti-cancer agent
- Review, Var, NA
antiOx↑, lycopene provides a strong antioxidant activity that is 100 times more effective than α-tocopherol and more than double effective that of β-carotene
TumCP↓, In vivo and in vitro experiments have demonstrated that lycopene at near physiological levels (0.5−2 μM) could inhibit cancer cell proliferation [[22], [23], [24]], induce apoptosis [[25], [26], [27]], and suppress metastasis [
Apoptosis↑,
TumMeta↑,
ChemoSen↑, lycopene can increase the effect of anti-cancer drugs (including adriamycin, cisplatin, docetaxel and paclitaxel) on cancer cell growth and reduce tumour size
BioAv↓, low water solubility and bioavailability of lycopene
Dose↝, The concentration of lycopene in plasma (daily intake of 10 mg lycopene) is approximately 0.52−0.6 μM
BioAv↓, significant decrease in lycopene bioavailability in the elderly
BioAv↑, oils and fats favours the bioavailability of lycopene [80], while large molecules such as pectin can hinder the absorption of lycopene in the small intestine due to their action on lipids and bile salt molecules
SOD↑, GC: 50−150 mg/kg BW/day ↑SOD, CAT, GPx ↑IL-2, IL-4, IL-10, TNF-α ↑IgA, IgG, IgM ↓IL-6
Catalase↑,
GPx↑,
IL2↑, lycopene treatment significantly enhanced blood IL-2, IL-4, IL-10, TNF-α levels and reduced IL-6 level in a dose-dependent manner.
IL4↑,
IL1↑,
TNF-α↑,
GSH↑, GC: ↑GSH, GPx, GST, GR
GPx↑,
GSTA1↑,
GSR↑,
PPARγ↑, ↑GPx, SOD, MDA ↑PPARγ, caspase-3 ↓NF-κB, COX-2
Casp3↑,
NF-kB↓,
COX2↓,
Bcl-2↑, AGS cells Lycopene 5 μM ↑Bcl-2 ↓Bax, Bax/Bcl-2, p53 ↓Chk1, Chk2, γ-H2AX, DNA damage ↓ROS Phase arrest
BAX↓,
P53↓,
CHK1↓,
Chk2↓,
γH2AX↓,
DNAdam↓,
ROS↓,
P21↑, CRC: ↑p21 ↓PCNA, β-catenin ↓COX-2, PGE2, ERK1/2 phosphorylated
PCNA↓,
β-catenin/ZEB1↓,
PGE2↓,
ERK↓,
cMyc↓, AGS cells: ↓Wnt-1, c-Myc, cyclin E ↓Jak1/Stat3, Wnt/β-catenin alteration ↓ROS
cycE/CCNE↓,
JAK1↓,
STAT3↓,
SIRT1↑, Huh7: ↑SIRT1 ↓Cells growth ↑PARP cleavage ↓Cyclin D1, TNFα, IL-6, NF-κB, p65, STAT3, Akt activation ↓Tumour multiplicity, volume
cl‑PARP↑,
cycD1/CCND1↓,
TNF-α↓,
IL6↓,
p65↓,
MMP2↓, SK-Hep1 human hepatoma cells Lycopene 5, 10 μM ↓MMP-2, MMP-9 ↓
MMP9↓,
Wnt↓, AGS cells Lycopene 0.5 μM, 1 μM ↓Wnt-1, c-Myc, cyclin E ↓Jak1/Stat3, Wnt/β-catenin alteration ↓ROS

1782- MEL,    Melatonin in Cancer Treatment: Current Knowledge and Future Opportunities
- Review, Var, NA
AntiCan↑, involvement of melatonin in different anticancer mechanisms
Apoptosis↑, apoptosis induction, cell proliferation inhibition, reduction in tumor growth and metastases
TumCP↓,
TumCG↑,
TumMeta↑,
ChemoSideEff↓, reduction in the side effects associated with chemotherapy and radiotherapy, decreasing drug resistance in cancer therapy,
radioP↑,
ChemoSen↑, augmentation of the therapeutic effects of conventional anticancer therapies
*ROS↓, directly scavenge ROS and reactive nitrogen species (RNS)
*SOD↑, melatonin can regulate the activities of several antioxidant enzymes like superoxide dismutase, glutathione reductase, glutathione peroxidase, and catalase
*GSH↑,
*GPx↑,
*Catalase↑,
Dose∅, demonstrated that 1 mM melatonin concentration is the pharmacological concentration that is able to produce anticancer effects
VEGF↓, downregulatory action on VEGF expression in human breast cancer cells
eff↑, tumor-bearing mice were treated with (10 mg/kg) of melatonin and (5 mg/kg) of cisplatin. The results have shown that melatonin was able to reduce DNA damage
Hif1a↓, MDA-MB-231-downregulation of the HIF-1α gene and protein expression coupled with the production of GLUT1, GLUT3, CA-IX, and CA-XII
GLUT1↑,
GLUT3↑,
CAIX↑,
P21↑, upregulation of p21, p27, and PTEN protein is another way of melatonin to promote cell programmed death in uterine leiomyoma
p27↑,
PTEN↑,
Warburg↓, FIGURE 3
PI3K↓, in colon cancer cells by downregulation of PI3K/AKT and NF-κB/iNOS
Akt↓,
NF-kB↓,
cycD1/CCND1↓,
CDK4↓,
CycB/CCNB1↓,
CDK4↓,
MAPK↑,
IGF-1R↓,
STAT3↓,
MMP9↓,
MMP2↓,
MMP13↓,
E-cadherin↑,
Vim↓,
RANKL↓,
JNK↑,
Bcl-2↓,
P53↑,
Casp3↑,
Casp9↑,
BAX↑,
DNArepair↑,
COX2↓,
IL6↓,
IL8↓,
NO↓,
T-Cell↑,
NK cell↑,
Treg lymp↓,
FOXP3↓,
CD4+↑,
TNF-α↑,
Th1 response↑, FIGURE 3
BioAv↝, varies 1% to 50%?
RadioS↑, melatonin’s radio-sensitizing properties
OS↑, In those individuals taking melatonin, the overall tumor regression rate and the 5-year survival were elevated

4697- PTS,    Pterostilbene and cancer: current review
- Review, Var, NA
TumCCA↑, pterostilbene inhibits cancer growth through alteration of the cell cycle, induction of apoptosis, and inhibition of metastasis
Apoptosis↑,
TumMeta↑,
toxicity↓, with negligible toxicity
BioAv↑, pterostilbene exhibits much greater bioavailability compared with other stilbene compounds

3105- VitC,    ROS-lowering doses of vitamins C and A accelerate malignant melanoma metastasis
- Review, Var, NA
TumMeta↑, Our current finding that also VitC and the two Vitamin A-related compounds β-carotene and retinyl palmitate can accelerate melanoma metastasis suggest that several antioxidant compounds relevant to the human diet have the capacity to spread tumors.

1755- WBV,    Reduction of breast cancer extravasation via vibration activated osteocyte regulation
Dose∅, However, intense exercise is physically challenging for bedridden, disabled, or aged patients. As an exercise surrogate, low-magnitude (<1 g) high-frequency (>30 Hz) (LMHF) vibration has gained growing interest
TumMeta↑, These data indicated that LMHF vibration could inhibit cancer extravasation, suggesting that vibration may suppress bone metastasis in breast cancer patients.
eff∅, Nevertheless, recent clinical studies indicated that LMHF vibration had minimum or no beneficial effects for the elderly (>65 years old)
Piezo1↑, LMHF vibration (60 Hz, 0.3 g, 1 h, Figure 1) significantly up-regulated the expressions of Piezo1 (1.63-fold) and COX-2 (1.32-fold) and down-regulated the expression of RANKL (0.86-fold).
COX2↑,
RANKL↓, down-regulated the expression of RANKL (0.86-fold).
TumCG∅, Vibration (60 Hz, 0.3 g, 1 h/day for 3 days) did not significantly impact cell growth and viability
tumCV∅,
TumCI↓, Vibration reduced breast cancer invasion via direct and indirect osteocyte signaling. vibration decreased cancer invasion distance by 24%


Showing Research Papers: 1 to 9 of 9

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   Fenton↑, 1,   GPx↑, 2,   GSH↓, 1,   GSH↑, 1,   GSR↑, 1,   GSTA1↑, 1,   NRF2↓, 1,   ROS↓, 1,   ROS↑, 2,   SOD↑, 1,  

Mitochondria & Bioenergetics ⓘ

XIAP↓, 2,  

Core Metabolism/Glycolysis ⓘ

CAIX↑, 1,   cMyc↓, 2,   PPARγ↑, 1,   SIRT1↑, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 5,   Bak↑, 1,   BAX↓, 1,   BAX↑, 2,   Bcl-2↓, 2,   Bcl-2↑, 1,   Bcl-xL↓, 1,   BIM↑, 1,   Casp↑, 1,   Casp3↑, 3,   Casp9↑, 2,   Chk2↓, 1,   JNK↑, 1,   MAPK↑, 1,   NOXA↑, 1,   p27↑, 1,   PUMA↑, 1,   survivin↓, 2,   TRAIL↑, 1,  

Transcription & Epigenetics ⓘ

tumCV∅, 1,  

DNA Damage & Repair ⓘ

CHK1↓, 1,   DNAdam↓, 1,   DNArepair↑, 1,   DNMTs↓, 1,   P53↓, 1,   P53↑, 2,   cl‑PARP↑, 2,   PCNA↓, 1,   γH2AX↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 2,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 3,   cycE/CCNE↓, 1,   P21↑, 3,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

EMT↑, 1,   ERK↓, 1,   HDAC↓, 1,   HDAC8↓, 1,   IGF-1R↓, 1,   PI3K↓, 1,   Piezo1↑, 1,   PTEN↑, 1,   SCF↓, 1,   STAT3↓, 4,   STAT3↑, 1,   TumCG↑, 1,   TumCG∅, 1,   Wnt↓, 1,  

Migration ⓘ

AP-1↓, 1,   E-cadherin↑, 1,   Ki-67↑, 1,   MMP13↓, 1,   MMP2↓, 3,   MMP9↓, 2,   MMP9↑, 1,   MMPs↓, 1,   Treg lymp↓, 1,   TumCI↓, 2,   TumCI↑, 1,   TumCMig↑, 1,   TumCP↓, 4,   TumMeta↑, 9,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   Hif1a↓, 2,   NO↓, 1,   VEGF↓, 3,  

Barriers & Transport ⓘ

GLUT1↑, 1,   GLUT3↑, 1,  

Immune & Inflammatory Signaling ⓘ

CD4+↑, 1,   COX2↓, 2,   COX2↑, 1,   FOXP3↓, 1,   IL1↑, 1,   IL2↑, 1,   IL4↑, 1,   IL6↓, 2,   IL8↓, 1,   JAK1↓, 1,   NF-kB↓, 3,   NK cell↑, 1,   p65↓, 1,   PGE2↓, 1,   T-Cell↑, 1,   Th1 response↑, 1,   TNF-α↓, 1,   TNF-α↑, 2,  

Hormonal & Nuclear Receptors ⓘ

RANKL↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 3,   BioAv↑, 2,   BioAv↝, 1,   ChemoSen↑, 3,   Dose↝, 1,   Dose∅, 2,   eff↑, 2,   eff∅, 1,   Half-Life↓, 1,   RadioS↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

IL6↓, 2,   Ki-67↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   chemoPv↑, 1,   ChemoSideEff↓, 1,   OS↑, 1,   radioP↑, 1,   toxicity↓, 1,  
Total Targets: 129

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   GSH↑, 2,   GSTs↑, 1,   ROS↓, 3,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

NADPH↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↑, 1,   NF-kB↓, 1,  

Functional Outcomes ⓘ

toxicity↓, 1,  
Total Targets: 11

Scientific Paper Hit Count for: TumMeta, Cancer Metastasis
1 Capsaicin
1 Chrysin
1 Curcumin
1 Ginkgo biloba
1 Lycopene
1 Melatonin
1 Pterostilbene
1 Vitamin C (Ascorbic Acid)
1 Whole Body Vibration
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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