TumMeta Cancer Research Results
TumMeta, Cancer Metastasis: Click to Expand ⟱
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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.
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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↑,
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.
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
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AD, |
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*toxicity↑, The emergence of natural products has provided extremely valuable references for the treatment of various diseases. Cucurbitacin B, a tetracyclic triterpenoid compound isolated from cucurbitaceae and other plants, is the most abundant member of the c
*antiOx↑, cucurbitacin B and cucurbitacin I have antioxidant properties, which can inhibit lipid peroxides
*Inflam↓, These results suggest that cucurbitacin B can inhibit the activation of NLRP3 inflammasome to inhibit the inflammatory response and cell damage in brain I/R injury.
*NLRP3↓,
*NF-kB↓, cucurbitacins B, E, and I can significantly reduce the activation activity of NF-κB induced by TLR 2/4 agonists in cells.
*neuroP↑, administration of cucurbitacin B has been shown to enhance the generation of new neurons in the hippocampus of ICR and APP/PS1 mice, thereby ameliorating the working memory deficits observed in these mice models
*memory↑,
*GABA↑, Concurrently, cucurbitacin B enhanced the levels of GABA.
*cardioP↑, cucurbitacin B exerts protective effects on the heart, including the prevention of hypertrophy, the amelioration of compromised cardiac function following myocardial infarction,
AntiTum↑, Cucurbitacin B has cytotoxic activity on a variety of tumor cells (Figure 5), and it has a good clinical application prospect as an antitumor drug.
p‑FAK↓, cucurbitacin B inhibited the phosphorylation of FAK and paxillin, and it could also induce the production of reactive oxygen species (ROS), which is helpful for the anti-metastatic potential of the cells.
ROS↑,
TumMeta↑,
TumCP↓, cucurbitacin B induced early apoptosis in these cells and altered the expression of proteins involved in proliferation and apoptosis, such as up-regulating the p53 and p21 genes.
Apoptosis↑,
P53↑,
P21↑,
TumCCA↑, cucurbitacin B affected the cell cycle transition from the G0/G1 phase to the S phase.
p27↑, cucurbitacin B upregulated the expression of p27 and downregulated the expression of CDK4, CDK2, cyclin D1, and cyclin E mRNA.
CDK4↓,
CDK2↓,
cycD1/CCND1↓,
cycE/CCNE↓,
STAT3↓, inhibiting the STAT3 signaling pathway
ChemoSen↑, combination of cucurbitacin B and cisplatin (DDP) enhanced the activation of caspase-3 and the cleavage of caspase-3 substrate PARP, and it decreased the expression level of pSTAT3.
MMP2↓, It may down-regulate the expression of MMP2, MMP9, and VEGF, which could significantly inhibit cell migration and angiogenesis.
MMP9↓,
VEGF↓,
TumCMig↓,
angioG↓,
NOTCH↓, the Notch signaling pathway in LNCaP cells was down-regulated.
EMT↓, Additionally, it inhibits the epithelial–mesenchymal transition (EMT) mediated by TGF-β1
toxicity↑, Cucurbitacin B exhibits good activity against HepG2 cells, but its high toxicity results in a low therapeutic index (TI).
BioAv↑, Cu-B SLNs can passively target tumors with the EPR effect and show higher accumulation in tumor interstitial space, which can improve the efficacy of cucurbitacin B and reduce the dose.
EPR↑,
*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.
TumCP↓, Deguelin demonstrates anticancer activity by suppressing cell proliferation and promoting apoptosis via the modulation of critical signaling pathways, such as NF-κB, Wnt, and AMPK pathways.
Apoptosis↑,
NF-kB↓, Several studies have shown that deguelin treatment can inhibit NF-κB activation, thereby inducing apoptosis in multiple cell types.
Wnt↓,
TumCCA↑, including cell cycle arrest, autophagy modulation, anti-angiogenic and anti-metastatic capabilities, along with antioxidant and anti-inflammatory actions.
TumMeta↑,
antiOx↑,
Inflam↓,
angioG↓, deguelin can inhibit angiogenesis and tumor metastasis through a variety of targets, such as MMPs, HIF-1α, FAK and PI3K/Akt pathway
Half-Life↑, . It exhibited a long mean residence time (6.98 h) and a terminal half-life of 9.26 h, supporting its potential for once-daily dosing.
MMP2↓, deguelin reduced the expression of MMP-2 and MMP-9
MMP9↓,
Casp9↑, deguelin can also induce apoptosis of gastric cancer cells through the activation of two key apoptotic pathways, caspase-9 and caspase-3
Casp3↑,
EMT↓, (NSCLC) mouse model, deguelin was found to inhibit the EMT process by promoting the expression of PTEN and KLF4,
PTEN↑,
ChemoSen↑, Its combination with conventional chemotherapy has also been shown to enhance the efficacy
toxicity↑, Long-term or high-dose deguelin administration induces a Parkinson’s disease-like condition in rats
*BBB↑, findings indicate that both deguelin and L80 can effectively penetrate the blood-brain barrier (BBB).
TumCG↓, Dipyridamole significantly reduced primary tumor growth and metastasis formation by intraperitoneal administration.
TumMeta↑, Experimental metastasis assays show dipyridamole reduces metastasis formation by 47.5 % in the MDA-MB-231T xenograft model
β-catenin/ZEB1↓, In vivo dipyridamole decreased activated β-catenin
*AntiAg↑, dipyridamole (Persantin Retard 200 mg) in combination with aspirin (25 mg) has been designed to take advantage of the additive antiplatelet effects of both of these agents, and this combination is used for secondary stroke prevention
TumCCA↑, In this study we further confirm the dipyridamole induces in vitro G1 cell cycle arrest in breast cancer cells and provide evidence that dipyridamole impairs in vivo the breast cancer tumor growth
Wnt↓, dipyridamole can attenuate the Wnt signaling pathway, through reduced β-catenin activation
NF-kB↓, ability of dipyridamole to decrease the activation of the Wnt, ERK1/2-MAPK and NF-kB signaling pathways.
AntiCan↑, It has therapeutic effects in cancer, diabetes, neurodegenerative diseases or chronic inflammatory diseases.
*AntiDiabetic↑, anticancer, neuroprotective, antidiabetic, antioxidant and anti-inflammatory.
*neuroP↑,
*Inflam↓,
*antiOx↑,
*BioAv↓, Because its bioavailability is low, there are limitations in clinical therapeutic use.
*BioAv↑, combined administration of emodin and piperine has been observed to clinically improve emodin pharmacokinetics, increasing 221 % of the area under the curve (AUC), 258 % the maximum concentration (Cmax), and decreasing 230 % the clearance related to
*SOD↑, fig 2 antioxidant
*GPx↑,
*GSH↑,
*NRF2↑,
*ROS↓,
*lipid-P↓,
*Cyt‑c↓,
*BAX↓, fig 2 antiinflammatory
*Bcl-2↓,
*iNOS↓,
*NO↓,
*IL6↓,
*IL10↓,
*IL17↓,
*IFN-γ↓,
*NF-kB↓,
*LC3II↓,
*Akt↓,
*Beclin-1↓,
*AMPK↓, fig 2 neuroprotective
*TNF-α↓,
*PGE2↓,
*Apoptosis↓,
*Casp3↓,
*Casp9↓,
*P53↓,
*P21↓,
*NAD↓, neuronal oxidative stress
*ATP↓,
*CHOP↓,
*GADD34↓,
*ATF4↓,
tumCV↓, fig 2 anticancer
Apoptosis↑,
TumCG↓,
TumCI↓,
TumMeta↓,
CSCs↓, glioma stem cells ↓b-catenin, ↓Notch-1, ↓STAT3
NOTCH1↓,
STAT3↓,
eff↑, emodin combined with curcumin ↓proliferation, ↑miR-34a
miR-34a↓,
*neuroP↑, Neuroprotective LPS-stimulated mouse ↓Nrf-2, NQO1, ↓TNF-α,↓↓ IL-6, ↓NO, ↓PGE2
*BDNF↓, model of chronic stress mice in vivo ↓progression of behavioral impairments in mice ↓consumption of sucrose, ↓plasmatic corticosterone, ↓mRNA, ↓BDNF,
*hepatoP↑, Hepatoprotective rats in vivo ↓ethanol-mediated liver steatosis ↓ ALT, ↓AST, ↓ TGL
*ALAT↓,
*AST↓,
TG/TAG↓,
ROS↑, However, at higher concentrations, emodin significantly increased ROS generation and reduced cell viability.
Slug↓, expression levels of Slug (a transcription factor) were also suppressed with emodin treatment.
EMT↓, results suggested that emodin suppressed the epithelial-mesenchymal transition of cancer cells through the ILK/GSK-3β/Slug signaling pathway
Glycolysis↓, In addition, emodin inhibited glycolysis via ROS-induced inactivation of the PI3K/AKT signaling pathway.
ChemoSen↑, The study by Peng et al. [130] also showed chemosensitizing effects of emodin to cisplatin in A549 (2–20 µM, for 48 h) and H460 (0.5–10 µM) non-small cell lung cancer cells.
P-gp↓, The sensitization mechanism was mediated by the inhibition of P-glycoprotein (Pgp), a drug-resistant protein related to the efflux pump mechanism.
Ki-67↓, The significant reduction of Ki-67 and proliferating cell nuclear antigen (PCNA) protein levels supported the antiproliferative effect of emodin in animal models.
PCNA↓,
ER Stress↑, findings suggested that emodin exerts its apoptotic effects in a process mediated by ER stress and the activation of the TRIB3/NF-κB pathway in lung cancer cells.
TRIB3↑,
NF-kB↑,
TumMeta↑, Emodin (40 mg/kg for 7 days) significantly decreased the metastatic recurrence of breast cancer after surgery in the lungs by reducing the formation of epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC).
*Imm↓, emodin may be developed as an immunosuppressive agent in case of immune activation, autoimmune disorders even in organ transplantation
*toxicity↝, An excess of emodin due to its laxative effects causes intestinal pain and severe diarrhea with subsequent electrolyte imbalance and dehydration [157]. Therefore, treatment should begin when symptoms appear, with special attention to electrolyte leve
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
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
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
TumCP↓, anti-proliferation, induction of apoptosis, inhibition of metastasis and angiogenesis, and modulation of carcinogen-metabolizing enzymes.
Apoptosis↓,
TumMeta↑,
angioG↓,
*antiOx↑, nimbolidehas been found to possess antioxidant effect and free radical scavenging activities.
*eff↑, In comparison to azadirachtin and ascorbic acid (vitamin C), nimbolide was shown to be a more potent antioxidant
Apoptosis↑, Nimbolide induces apoptosis through diverse molecular mechanism(s).
MOMP↑, Nimbolide disrupts MOMP, which promotes caspases activation leading to apoptosis.
CDK1↓, Nimbolide also reduces the level of CDKs and cyclins, causing cell cycle arrest.
TumCCA↑,
MAPK↓, Nimbolide also abrogates various signaling cascades including MAPK (ERK1/2), JAK2/STAT3 and PI3K/Akt, leading to suppression of proliferation of a wide variety of human cancer cells.
JAK2↓,
STAT3↓,
PI3K↓,
Akt↓,
TumCP↓,
*NRF2↑, Nimbolide disrupts the Nrf2-KEAP1 complex and promotes the release of Nrf2, thus increasing levels of antioxidant and detoxification enzymes.
NF-kB↓, Inhibition of the NF-κB pathway also reduces the dissociation of GSK-3β from β-catenin, hence restraining the Wnt/β-catenin
GSK‐3β↑,
Wnt↓,
β-catenin/ZEB1↓,
chemoPv↑, nimbolide showed remarkable chemopreventive property.
Bcl-xL↓, Nimbolide treatmentdecreased the expression of antiapoptotic proteins(Bcl-xL, Bcl-2, survivin, caspase inhibitor molecules) and increased the expression of proapoptotic proteins (cytochrome c, Bax, Bad, Bid, cleaved caspases) in prostate cancer cells
Bcl-2↓,
survivin↓,
Cyt‑c↑,
BAX↑,
BID↑,
cl‑Casp↑,
P53↑, nimbolide acted by up-regulation of p53 levelin HeLa cells, thereby priming these cells towards apoptosis by destabilizing the mitochondria
DR5↑, Nimbolide up-regulated the expression of both DR5 and DR4 in chronic myeloid leukemia (KBM-5), multiple myeloma (U266), embryonic kidney carcinoma (A293), pancreatic adenocarcinoma (AsPC-1), and breast adenocarcinoma (MDA-MB-231) cells
DR4↑,
ROS↑, nimbolide resulted in generation of reactive oxygen species (ROS)
lipid-P↑, ROS also induced lipid peroxidation of cellular membranes, generating toxic metabolites such as malondialdehyde (MDA) that can react with DNA to form adducts to induce apoptosis.
MDA↑,
MMP2↓, nimbolide reduced mRNA expression of MMP-2, MMP-9, uPA and uPA receptor in breast cancer cells (MCF-7)
MMP9↓,
uPA↓,
ICAM-1↓, nimbolide was shown to downregulate the expression of MMP-9, ICAM-1, and CXCR4 in colorectal cancer xenografts
CXCR4↓,
CXCR2↓, nimbolide also reduced expression of CXCL8 and CXCR2 in breast cancers, and thus abrogated angiogenesis
angioG↓,
BBB↑, nimbolide might be able to cross blood-brain barrier (BBB) and the concentration could be sufficient for nimbolide to suppress intracranial tumour cell proliferation.
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
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.
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 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(tgid=1) ⓘ
antiOx↑, 2, Catalase↑, 1, Fenton↑, 2, Ferroptosis↑, 1, GPx↑, 2, GSH↓, 1, GSH↑, 1, GSR↑, 1, GSTA1↑, 1, lipid-P↑, 2, MDA↑, 1, NRF2↓, 1, ROS↓, 1, ROS↑, 6, SOD↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↓, 1, ETC↓, 1, MMP↓, 1, MPT↑, 1, XIAP↓, 2,
Core Metabolism/Glycolysis(tgid=4) ⓘ
CAIX↑, 1, cMyc↓, 2, Glycolysis↓, 1, PPARγ↑, 1, SIRT1↑, 1, Warburg↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 3, Apoptosis↓, 1, Apoptosis↑, 10, Bak↑, 1, BAX↓, 1, BAX↑, 3, Bcl-2↓, 3, Bcl-2↑, 1, Bcl-xL↓, 2, BID↑, 1, BIM↑, 1, Casp↑, 2, cl‑Casp↑, 1, Casp3↑, 4, Casp9↑, 3, Chk2↓, 1, Cupro↑, 1, Cyt‑c↑, 2, DR4↑, 1, DR5↑, 1, Ferroptosis↑, 1, JNK↑, 1, MAPK↓, 1, MAPK↑, 1, MOMP↑, 1, NOXA↑, 1, p27↑, 2, PUMA↑, 1, survivin↓, 3, TRAIL↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
tumCV↓, 1, tumCV∅, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
CHK1↓, 1, DNAdam↓, 1, DNArepair↑, 1, DNMTs↓, 1, P53↓, 1, P53↑, 4, cl‑PARP↑, 2, PCNA↓, 2, γH2AX↓, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK1↓, 1, CDK2↓, 2, CDK4↓, 3, CycB/CCNB1↓, 1, cycD1/CCND1↓, 4, cycE/CCNE↓, 2, P21↑, 4, TumCCA↑, 7,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
CSCs↓, 1, EMT↓, 3, EMT↑, 1, ERK↓, 1, GSK‐3β↑, 1, HDAC↓, 1, HDAC8↓, 1, IGF-1R↓, 1, miR-34a↓, 1, NOTCH↓, 1, NOTCH1↓, 1, PI3K↓, 2, Piezo1↑, 1, PTEN↑, 2, SCF↓, 1, STAT3↓, 7, STAT3↑, 1, TumCG↓, 3, TumCG↑, 1, TumCG∅, 1, Wnt↓, 4,
Migration(tgid=13) ⓘ
AP-1↓, 1, Ca+2↑, 1, E-cadherin↑, 1, p‑FAK↓, 1, Ki-67↓, 1, Ki-67↑, 1, MMP13↓, 1, MMP2↓, 6, MMP9↓, 5, MMP9↑, 1, MMPs↓, 1, Slug↓, 1, Treg lymp↓, 1, TRIB3↑, 1, TumCI↓, 3, TumCI↑, 2, TumCMig↓, 1, TumCMig↑, 2, TumCP↓, 8, TumCP↑, 1, TumMeta↓, 1, TumMeta↑, 15, uPA↓, 1, Vim↓, 1, β-catenin/ZEB1↓, 3,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 6, angioG↑, 1, EPR↑, 1, Hif1a↓, 2, NO↓, 1, VEGF↓, 4,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 1, GLUT1↑, 1, GLUT3↑, 1, P-gp↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CD4+↑, 1, COX2↓, 2, COX2↑, 1, CXCR2↓, 1, CXCR4↓, 1, FOXP3↓, 1, ICAM-1↓, 1, IL1↑, 1, IL2↑, 1, IL4↑, 1, IL6↓, 2, IL8↓, 1, Inflam↓, 1, JAK1↓, 1, JAK2↓, 1, NF-kB↓, 6, NF-kB↑, 1, NK cell↑, 1, p65↓, 1, PGE2↓, 1, T-Cell↑, 1, Th1 response↑, 1, TNF-α↓, 1, TNF-α↑, 2,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
RANKL↓, 2,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 3, BioAv↑, 3, BioAv↝, 1, ChemoSen↑, 6, DDS↑, 1, Dose↝, 1, Dose∅, 2, eff↑, 4, eff∅, 1, Half-Life↓, 1, Half-Life↑, 1, RadioS↑, 1, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
IL6↓, 2, Ki-67↓, 1, Ki-67↑, 1, TG/TAG↓, 1, TRIB3↑, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 2, AntiTum↑, 1, chemoPv↑, 2, ChemoSideEff↓, 1, OS↑, 1, radioP↑, 1, toxicity↓, 1, toxicity↑, 2,
Total Targets: 183
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 4, Catalase↑, 1, GPx↑, 2, GSH↑, 3, GSTs↑, 1, lipid-P↓, 1, NRF2↑, 2, ROS↓, 4, SOD↑, 2,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 1, AMPK↓, 1, NAD↓, 1, NADPH↑, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 1, Apoptosis↓, 1, BAX↓, 1, Bcl-2↓, 1, Casp3↓, 1, Casp9↓, 1, Cyt‑c↓, 1, GADD34↓, 1, iNOS↓, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP↓, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
Beclin-1↓, 1, LC3II↓, 1,
DNA Damage & Repair(tgid=10) ⓘ
P53↓, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
P21↓, 1,
Migration(tgid=13) ⓘ
AntiAg↑, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
ATF4↓, 1, NO↓, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
IFN-γ↓, 1, IL10↓, 1, IL17↓, 1, IL6↓, 1, Imm↓, 1, Inflam↓, 2, Inflam↑, 1, NF-kB↓, 3, PGE2↓, 1, TNF-α↓, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
BDNF↓, 1, GABA↑, 1,
Protein Aggregation(tgid=19) ⓘ
NLRP3↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1, BioAv↑, 1, eff↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, AST↓, 1, IL6↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiDiabetic↑, 1, cardioP↑, 1, hepatoP↑, 1, memory↑, 1, neuroP↑, 3, toxicity↓, 1, toxicity↑, 1, toxicity↝, 1,
Total Targets: 59
Scientific Paper Hit Count for: TumMeta, Cancer Metastasis
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#:604 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
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