TumCA Cancer Research Results
TumCA, Tumor Cell adhesion: Click to Expand ⟱
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Tumor Cell adhesion
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Scientific Papers found: Click to Expand⟱
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in-vitro, |
Colon, |
Caco-2 |
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in-vitro, |
Colon, |
HT29 |
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in-vitro, |
CRC, |
LoVo |
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Apoptosis↑, CA induced cell death by apoptosis in Caco-2 line after 24 h of treatment and inhibited cell adhesion and migration,
TumCMig↓, Inhibition of cell migration by CA
uPA↓, possibly by reducing the activity of secreted proteases such as urokinase plasminogen activator (uPA) and metalloproteinases (MMPs).
MMPs↓,
COX2/PTGS2↓, we have determined that CA downregulates the expression of COX-2 in Caco-2 cells at both the mRNA and protein levels.
TumCA↓, Inhibition of cell adhesion by CA
MMP9↓, CA treatment after 24 h decreased Caco-2 conditioned media uPA activity and MMP-9 and MMP-2.
MMP2↓,
chemoPv↑, CA may serve as chemopreventive and/or chemotherapeutic agent against colorectal cancer progress.
toxicity↓, CUSP9v3 is safe in patients with recurrent GBM.
TrxR↓, The anti-rheumatoid arthritis drug auranofin inhibits thioredoxin reductase, resulting in increased intracellular reactive oxygen species
ROS↓,
TumCI↓, The anti-hypertensive captopril reduces invasion, migration and adhesion of GBM cell activity through soluble matrix metalloproteinase (MMP)-2 and MMP-9 inhibition.12
TumCMig↓,
TumCA↓,
MMP2↓,
MMP9↓,
COX2/PTGS2↓, celecoxib has long been shown to have anticancer properties related to cyclooxygenase-2 inhibition and has demonstrated encouraging results in combination with low-dose temozolomide
ALDH↓, alcohol deterrent disulfiram is consistently cytotoxic to a wide range of cancer cells and is effective against GBM stem cells through aldehyde dehydrogenase inhibition.15
TumAuto↑, itraconazole likely exerts its anticancer activity due to its multiple pharmacological effects16 with specific data in GBM pointing towards an effect on autophagy
P-gp/ABCB1↓, the antidepressant sertraline was included for its ability to inhibit P-glycoprotein at the blood-brain barrier21
eff↑, Best overall response was stable disease (SD) in 6 patients and progressive disease (PD) in 4 patients
Src↓, The novel SFK/Abl inhibitor, dasatinib (BMS-354825), is a promising therapeutic agent with oral bioavailability.
ABL1↓,
BioAv↑,
TumCG↓, Dasatinib has been shown to inhibit growth of Bcr-Abl-dependent chronic myeloid leukemia xenografts in nude mice.
Dose↓, In this study, we show that dasatinib blocks the kinase activities of the SFKs, Lyn, and Src, in human prostate cancer cells at low nanomolar concentrations.
TumCA↓, Consistent with inhibition of these signaling pathways, dasatinib suppresses cell adhesion, migration, and invasion of prostate cancer cells at low nanomolar concentrations.
TumCMig↓,
TumCI↓,
DNAdam↑, Fisetin induced DNA fragmentation, ROS generation, and apoptosis in NCI-H460 cells via a reduction in Bcl-2 and increase in Bax expression
ROS↑,
Apoptosis↑,
Bcl-2↓,
BAX↑,
cl‑Casp9↑, Fisetin treatment increased cleavage of caspase-9 and caspase-3 thereby increasing caspase-3 activation
cl‑Casp3↑,
Cyt‑c↑, leading to cytochrome-c release
lipid-P↓, Fisetin (25 mg/kg body weight) decreased histological lesions and levels of lipid peroxidation and modulated the enzymatic and nonenzymatic anti-oxidants in B(a)P-treated Swiss Albino mice
TumCG↓, We observed that fisetin treatment (5–20 μM) inhibits cell growth and colony formation in A549 NSC lung cancer cells.
TumCA↓, Another study showed that fisetin inhibits adhesion, migration, and invasion in A549 lung cancer cells by downregulating uPA, ERK1/2, and MMP-2
TumCMig↓,
TumCI↓,
uPA↓,
ERK↓,
MMP9↓,
NF-kB↓, Treatment with fisetin also decreased the nuclear levels of NF-kB, c-Fos, c-Jun, and AP-1 and inhibited NF-kB binding.
cFos↓,
cJun↓,
AP-1↓,
TumCCA↑, Our laboratory has previously shown that treatment of LNCaP cells with fisetin caused inhibition of PCa by G1-phase cell cycle arrest
AR↓, inhibited androgen signaling and tumor growth in athymic nude mice
mTORC1↓, induced autophagic cell death in PCa cells through suppression of mTORC1 and mTORC2
mTORC2↓,
TSC2↑, activated the mTOR repressor TSC2, commonly associated with inhibition of Akt and activation of AMPK
EGF↓, Fisetin also inhibits EGF and TGF-β induced YB-1 phosphorylation and EMT in PCa cells
TGF-β↓,
EMT↓, Fisetin also inhibits EGF and TGF-β induced YB-1 phosphorylation and EMT in PCa cells
P-gp/ABCB1↓, decrease the P-gp protein in multidrug resistant NCI/ADR-RES cells.
PI3K↓, Fisetin also inhibited the PI3K/AKT/NFkB signaling
Akt↓,
mTOR↓, Fisetin inhibited melanoma progression in a 3D melanoma skin model with downregulation of mTOR, Akt, and upregulation of TSC
eff↑, combinational treatment study of melatonin and fisetin demonstrated enhanced antitumor activity of fisetin
ROS↓, Fisetin inhibited ROS and augmented NO generation in A375 melanoma cells
ER Stress↑, induction of ER stress evidenced by increased IRE1α, XBP1s, ATF4, and GRP78 levels in A375 and 451Lu cells.
IRE1↑,
ATF4↑,
GRP78/BiP↑,
ChemoSen↑, combination of fisetin with sorafenib effectively inhibited EMT and augmented the anti-metastatic potential of sorafenib by reducing MMP-2 and MMP-9 proteins in melanoma cell xenografts
CDK2↓, Fisetin (0–60 μM) was shown to inhibit activity of CDKs dose-dependently leading to cell cycle arrest in HT-29 human colon cancer cells
CDK4↓, Fisetin treatment decreased activities of CDK2 and CDK4 via decreased levels of cyclin-E, cyclin-D1 and increase in p21 (CIP1/WAF1) levels.
cycE/CCNE↓,
cycD1/CCND1↓,
P21↑,
COX2/PTGS2↓, fisetin (30–120 μM) induces apoptosis in colon cancer cells by inhibiting COX-2 and Wnt/EGFR/NF-kB -signaling pathways
Wnt↓,
EGFR↓,
β-catenin/ZEB1↓, Fisetin treatment inhibited Wnt/EGFR/NF-kB signaling via downregulation of β-catenin, TCF-4, cyclin D1, and MMP-7
TCF-4↓,
MMP7↓,
RadioS↑, fisetin treatment was found to radiosensitize human colorectal cancer cells which are resistant to radiotherapy
eff↑, Combined treatment of fisetin with NAC increased cleaved caspase-3, PARP, reduced mitochondrial membrane potential with induction of caspase-9 in COLO25 cells
other↝, Except in China, where gossypol is available on the drug market as an adjuvant used for tumour treatment [85], in the rest of the world, gossypol is still under clinical trials investigation.
BioAv↑, To improve the water solubility and bioavailability of gossypol, Wang et al. [76] used gossypol-loaded pluronic F127 nanoparticles (GLPFNs), which increased bioavailability several times and exhibited higher organ uptake of the drug compared to using
Bcl-2↓, The main mechanism of gossypol-anticancer activity is inducing apoptosis through suppressing anti-apoptotic proteins of the Bcl-2 family.
Casp3↑, The caspase-dependent anti-tumour effect of gossypol is led by activation of caspase-3 and caspase-9.
Casp9↑,
MOMP↑, Apoptosis induced by independent pathways is made by alternations on the mitochondrial outer membrane permeabilisation
ROS↑, Gossypol treatment has been demonstrated to induce the production of reactive oxygen species (ROS) in tumour cell
ATP↓, 80 μmol/L gossypol resulted in a significant increase in cellular ROS levels, leading to ATP depletion, which induces mitochondrial dysfunction
mtDam↑,
Apoptosis↑, The impaired function of mitochondria further contributes to the activation of apoptosis
hTERT/TERT↓, ↓ decrease, telomerase reverse transcriptase (TERT)
Akt↓, ↓ decrease, telomerase reverse transcriptase (TERT), Adenosine triphosphate (ATP), Cellular myelocytomatosis oncogene (c-MyC), serine/threonine protein kinase (Akt)
TumAuto↑, Induction of autophagy as a complementary process of apoptosis
LC3‑Ⅱ/LC3‑Ⅰ↑, gossypol in colorectal cancer cells increased the LC3-II/LC3-I ratio and induced autophagy
NRF2↓, gossypol reduced Nrf2 protein stability, leading to the inhibition of the Nrf2/ARE pathway, resulting in a significant decrease of cell viability in human cancer cells
ARE↓,
ICAM-1↓, Treating breast cancer cells with gossypol has been shown to block the binding of NF-κB to the promoter regions of ICAM-1, suppressing TNF-α-induced ICAM-1 expression.
CX43/GJA1↓, It down-regulates the expression of CX43, nuclear NF-κB, TNF-α, toll-like receptor 4 (TLR4), and interleukin-6 (IL-6) in these cells, indicating its potential anti-inflammatory and anti-apoptotic effects
NF-kB↓,
TLR4↓,
IL6↓,
Inflam↓,
CUL5↝, gossypol has been found to block the neddylation of cullin enzymes (CUL5 and CUL1) by directly binding to the SAG-CUL5 or RBX1-CUL1 complex.
CUL1↝,
NOXA↑, This leads to the accumulation of both the pro-apoptotic protein NOXA
TumCI↓, gossypol significantly reduced the invasion, migration, and adhesion of these cancer cells by suppressing the FAK pathway and ETM
TumCMig↓,
TumCA↓,
FAK↓,
MDM2↓, gossypol, the binding between the MDM2 protein and VEGF mRNA was disrupted in breast cancer cells [78]. As a result, the expression of MDM2 and VEGF proteins is significantly decreased.
VEGF↓,
angioG↓, anti-angiogenic mechanism of gossypol in cancer cells (Fig. 7).
HLA-I/II↑, gossypol has been found to increase the expression of HLA-I/II molecules
Imm↑, This immune modulation may contribute to its anti-cancer activity by enhancing immune recognition and response against tumour cells
Dose↝, phase III clinical trial performed between January 2014 and February 2017, gossypol acetate tablets (20 mg/tablet) produced by Xi’an Northern Pharmaceutical Co., Ltd were tested with a placebo in 102 patients with NSCLC
Glycolysis↓, Moreover, the treatment of boars with gossypol inhibited glycolysis and the respiratory chain, leading to a decrease in oxidative phosphorylation and adenosine triphosphate (ATP) synthesis, causing a decrease in energy supply and inhibition of sperm
OXPHOS↓,
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in-vitro, |
Colon, |
Caco-2 |
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AntiCan↑, Inositol hexaphosphate (IP6 phytic acid) has been recognized to have both preventive and therapeutic effects against various cancers including that of colon.
TumCA↓, IP6 has been demonstrated to inhibit cancer cell adhesion and migration.
TumCMig↓,
MMP13↓, A significant decrease in MMP-13, MMP-3, MMP-2, and TIMP-1 basal expression was achieved by IP6.
MMP3↓,
MMP2↓,
TIMP1↓,
MMP1↓, IP6 was also an efficient downregulator of MMP-1, MMP-9, and TIMP-2 genes transcription stimulated by IL-1β in 6 h lasting culture.
MMP9↓,
TIMP2↓,
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in-vitro, |
BC, |
MDA-MB-231 |
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TumCA↓, IP6 treatment caused a 65% reduction of cell adhesion to fibronection (p = 0.002) and a 37% reduction to collagen (p = 0.005).
MMP9↓, Additionally, IP6 significantly (p = 0.006) inhibited the secretion of matrix metalloproteinase (MMP)-9 as assessed by zymography.
AntiCan↑, From an anti-cancer perspective, lycopene is often associated with reduced risk of prostate cancer and people often look for it as a dietary supplement which may help to prevent cancer.
TumCP↓, Lycopene was known to be able to suppress cancerous cell proliferation, migration, invasion and adhesion activity in cell culture studies.
TumCMig↓,
TumCI↓,
TumCA↓,
ROS↓, Such suppression was often observed with changes of cancer-related gene expression and relief of oxidative stress
MMP2↓, In general, lycopene could suppress the expression of MMP-2, MMP-7, MMP-9, Sp1, IGF-1R, VEGF while increasing E-cadherin stabilization, connexin 43, nm23-H1, TIMP-1 and TIMP-2 levels
MMP7↓,
MMP9↓,
VEGF↓,
E-cadherin↑,
TIMP1↑,
TIMP2↑,
BioAv↝, it is recommended to avoid consumption of lycopene concurrently with high dietary fiber intake as several types of dietary fiber were found to be able to reduce the bioavailability of lycopene
*IL12↓, lycopene could suppress proinflammatory cytokines such as IL-12, TNF-α, IL-1, IL-1β, IL-6
*TNF-α↓,
*IL1↓,
*IL1β↓,
*IL6↓,
COX2/PTGS2↓, Sprague Dawley rat model, lycopene treatment after induction by azoxymethane caused suppression of aberrant crypt foci, preneoplastic lesion and biomarkers such as COX-2 and iNOS expression
iNOS↓,
*radioP↑, lycopene before induction of DNA damage via X-irradiation as lycopene treatment after irradiation failed to show such DNA protective effect
NF-kB↓, anti-cancer effect of lycopene was also observed in pancreatic cancer cells (PANC-1 cell line) whereby significant reduction of ROS, NF-κB and anti-apoptotic biomarkers (cIAP1, cIAP2 and survivin) was detected while an increment of caspase-3 and Bax:
survivin↓,
Casp3↑,
Bax:Bcl2↑,
ChemoSen↑, this study suggests that 5-FU combined with magnolol exerts a synergistic anti-cervical cancer effect by regulating the PI3K/AKT/mTOR and epithelial-mesenchymal transition (EMT) signaling pathways.
TumCP↓, magnolol strongly inhibited cervical cancer cell proliferation,
vinculin↓, down-regulating the expression of α-actinin, tensin-2 and vinculin
TumCA↓, magnolol enhanced inhibitory effect of 5-FU on the cell adhesion, migration and invasion.
TumCMig↓,
TumCI↓,
p‑Akt↓, phosphorylation of AKT and PI3K and the expression of mTOR were strongly inhibited by the combination of 5-FU and magnolol.
p‑PI3K↓,
mTOR↓,
E-cadherin↑, expression of E-cadherin and β-catenin was upregulated
β-catenin/ZEB1↑,
Snail↓, expression of Snail, Slug and vimentin was down-regulated by the 5-FU together with magnolol.
Slug↓,
TumCA↓, Shikonin (1 μm) inhibited significantly the adhesion, invasion and migratory ability of MGC-803 cells.
TumCI↓,
TumCMig↓,
MMP2↓, matrix metalloproteinases (MMP)-2, MMP-7, TLR2 and p65 NF-κB
MMP7↓,
TLR2↓,
p65↓,
NF-kB↓,
eff↑, In addition, the co-incubation of Shikonin and anti-TLR2/MG-132 has a significant stronger activity than anti-TLR2 or MG-132 alone.
ROS↑, Shikonin-induced ROS generation
Showing Research Papers: 1 to 10 of 10
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 10
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
CUL1↝, 1, CUL5↝, 1, CX43/GJA1↓, 1, HLA-I/II↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
ARE↓, 1, lipid-P↓, 1, NRF2↓, 1, OXPHOS↓, 1, ROS↓, 3, ROS↑, 3, TrxR↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ABL1↓, 1, ATP↓, 1, EGF↓, 1, mtDam↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
Glycolysis↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 2, p‑Akt↓, 1, Apoptosis↑, 3, BAX↑, 1, Bax:Bcl2↑, 1, Bcl-2↓, 2, Casp3↑, 2, cl‑Casp3↑, 1, Casp9↑, 1, cl‑Casp9↑, 1, Cyt‑c↑, 1, hTERT/TERT↓, 1, iNOS↓, 1, MDM2↓, 1, MOMP↑, 1, NOXA↑, 1, survivin↓, 1,
Kinase & Signal Transduction(tgid=6) ⓘ
TSC2↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
cJun↓, 1, other↝, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 1, GRP78/BiP↑, 1, IRE1↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
LC3‑Ⅱ/LC3‑Ⅰ↑, 1, TumAuto↑, 2,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK2↓, 1, CDK4↓, 1, cycD1/CCND1↓, 1, cycE/CCNE↓, 1, P21↑, 1, TumCCA↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ALDH↓, 1, cFos↓, 1, EMT↓, 1, ERK↓, 1, mTOR↓, 2, mTORC1↓, 1, mTORC2↓, 1, PI3K↓, 1, p‑PI3K↓, 1, Src↓, 1, TCF-4↓, 1, TumCG↓, 2, Wnt↓, 1,
Migration(tgid=13) ⓘ
AP-1↓, 1, E-cadherin↑, 2, FAK↓, 1, MMP1↓, 1, MMP13↓, 1, MMP2↓, 5, MMP3↓, 1, MMP7↓, 3, MMP9↓, 6, MMPs↓, 1, Slug↓, 1, Snail↓, 1, TGF-β↓, 1, TIMP1↓, 1, TIMP1↑, 1, TIMP2↓, 1, TIMP2↑, 1, TumCA↓, 10, TumCI↓, 7, TumCMig↓, 9, TumCP↓, 2, uPA↓, 2, vinculin↓, 1, β-catenin/ZEB1↓, 1, β-catenin/ZEB1↑, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 1, ATF4↑, 1, EGFR↓, 1, VEGF↓, 2,
Barriers & Transport(tgid=15) ⓘ
P-gp/ABCB1↓, 2,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 4, ICAM-1↓, 1, IL6↓, 1, Imm↑, 1, Inflam↓, 1, NF-kB↓, 4, p65↓, 1, TLR2↓, 1, TLR4↓, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
AR↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↑, 2, BioAv↝, 1, ChemoSen↑, 2, Dose↓, 1, Dose↝, 1, eff↑, 4, RadioS↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
AR↓, 1, EGFR↓, 1, hTERT/TERT↓, 1, IL6↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 2, chemoPv↑, 1, toxicity↓, 1,
Total Targets: 115
Pathway results for Effect on Normal Cells:
Immune & Inflammatory Signaling(tgid=16) ⓘ
IL1↓, 1, IL12↓, 1, IL1β↓, 1, IL6↓, 1, TNF-α↓, 1,
Clinical Biomarkers(tgid=22) ⓘ
IL6↓, 1,
Functional Outcomes(tgid=23) ⓘ
radioP↑, 1,
Total Targets: 7
Scientific Paper Hit Count for: TumCA, Tumor Cell adhesion
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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