COL3A1 Cancer Research Results
COL3A1, collagen3a: Click to Expand ⟱
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COL3A1 encodes a component of type III collagen—a major structural protein in the extracellular matrix.
Elevated COL3A1 expression has frequently been observed in solid tumors and is often associated with a desmoplastic response.
There is a recurring observation across multiple tumor types that increased COL3A1 expression in the tumor stroma is linked to worse clinical outcomes, including more advanced stage and lower survival rates.
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Scientific Papers found: Click to Expand⟱
*hepatoP↑, Curc and Lip acid can be considered as promising natural therapies against liver injury, induced by NHPA, through their antioxidant and antifibrotic actions.
*α-SMA↓, Curc and Lip acid reduced the expression of alpha-smooth muscle actin and collagen III, upregulated by NHPA intoxication
*COL3A1↓,
*ROS↓, scavenging activity to ROS and a capacity to regenerate endogenous antioxidants such as GSH, and vitamins C and E.
*GSH↑,
*ALAT↓, ALT, AST, and ALP activity levels compared to those of the control group. The use of NACS, Curc, and/or Lip acid significantly reduced the toxic effects of NHPA on those enzymes,
*AST↓,
*ALP↓,
*MDA↓, The combination therapy showed an apparent reduction in MDA level more than other treatments
TumCP↓,
TumCMig↓,
TumCCA↑, G0/G1 cell cycle arrest
MMP∅, Capsaicin did not provoke significant loss of MMP
MMP2↓,
MMP9↓,
α-SMA↓,
COL1A1↓,
COL3A1↓,
TIMP1↓,
*Fibronectin↓,
*α-SMA↓,
*COL1↓, collagen1a
*COL3A1↓,
*TGF-β↓,
*EMT↓,
*MMP2↓, PL produced a significant attenuation of the BDL-induced increase in MMP-2, α-SMA, collagen1a, and
collagen3a expressio
*α-SMA↓,
*Smad7↑, Smad7 protein expression was decreased in BDL mice whereas upon PL treatment, it increased significantly
*E-cadherin↑, oral administration of PL demonstrated a dose-dependent increase in expression of E-cadherin and reduction in vimentin and fibronectin
expression
*Vim↓,
*hepatoP↑, Our study displays that PL treatment is capable of restoring liver enzymes, suggesting a hepatoprotective potential of PL in liver injury markers
*antiOx↑, PL showed powerful antioxidant effects by attenuating oxidative-nitrosative stress and increasing intracellular antioxidant GSH levels in BDL liver.
*GSH↑,
*ROS↓,
ROS↑, decided by the availability of intracellular reduced glutathione (GSH),
GSH↓, extended exposure with high concentration of quercetin causes a substantial decline in GSH levels
Ca+2↝,
MMP↓,
Casp3↑, activation of caspase-3, -8, and -9
Casp8↑,
Casp9↑,
other↓, when p53 is inhibited, cancer cells become vulnerable to quercetin-induced apoptosis
*ROS↓, Quercetin (QC), a plant-derived bioflavonoid, is known for its ROS scavenging properties and was recently discovered to have various antitumor properties in a variety of solid tumors.
*NRF2↑, Moreover, the therapeutic efficacy of QC has also been defined in rat models through the activation of Nrf-2/HO-1 against high glucose-induced damage
HO-1↑,
TumCCA↑, QC increases cell cycle arrest via regulating p21WAF1, cyclin B, and p27KIP1
Inflam↓, QC-mediated anti-inflammatory and anti-apoptotic properties play a key role in cancer prevention by modulating the TLR-2 (toll-like receptor-2) and JAK-2/STAT-3 pathways and significantly inhibit STAT-3 tyrosine phosphorylation within inflammatory ce
STAT3↓,
DR5↑, several studies showed that QC upregulated the death receptor (DR)
P450↓, it hinders the activity of cytochrome P450 (CYP) enzymes in hepatocytes
MMPs↓, QC has also been shown to suppress metastatic protein expression such as MMPs (matrix metalloproteases)
IFN-γ↓, QC is its ability to inhibit inflammatory mediators including IFN-γ, IL-6, COX-2, IL-8, iNOS, TNF-α,
IL6↓,
COX2↓,
IL8↓,
iNOS↓,
TNF-α↓,
cl‑PARP↑, Induced caspase-8, caspase-9, and caspase-3 activation, PARP cleavage, mitochondrial membrane depolarization,
Apoptosis↑, increased apoptosis and p53 expression
P53↑,
Sp1/3/4↓, HT-29 colon cancer cells: decreased the expression of Sp1, Sp3, Sp4 mrna, and survivin,
survivin↓,
TRAILR↑, H460 Increased the expression of TRAILR, caspase-10, DFF45, TNFR 1, FAS, and decreased the expression of NF-κb, ikkα
Casp10↑,
DFF45↑,
TNFR 1↑,
Fas↑,
NF-kB↓,
IKKα↓,
cycD1/CCND1↓, SKOV3 Reduction in cyclin D1 level
Bcl-2↓, MCF-7, HCC1937, SK-Br3, 4T1, MDA-MB-231 Decreased Bcl-2 expression, increasedBax expression, inhibition of PI3K-Akt pathway
BAX↑,
PI3K↓,
Akt↓,
E-cadherin↓, MDA-MB-231 Induced the expression of E-cadherin and downregulated vimentin levels, modulation of β-catenin target genes such as cyclin D1 and c-Myc
Vim↓,
β-catenin/ZEB1↓,
cMyc↓,
EMT↓, MCF-7 Suppressed the epithelial–mesenchymal transition process, upregulated E-cadherin expression, downregulated vimentin and MMP-2 expression, decreased Notch1 expression
MMP2↓,
NOTCH1↓,
MMP7↓, PANC-1, PATU-8988 Decreased the secretion of MMP and MMP7, blocked the STAT3 signaling pathway
angioG↓, PC-3, HUVECs Reduced angiogenesis, increased TSP-1 protein and mrna expression
TSP-1↑,
CSCs↓, PC-3 and LNCaP cells Activated capase-3/7 and inhibit the expression of Bcl-2, surviving and XIAP in CSCs.
XIAP↓,
Snail↓, inhibiting the expression of vimentin, slug, snail and nuclear β-catenin, and the activity of LEF-1/TCF responsive reporter
Slug↓,
LEF1↓,
P-gp↓, MCF-7 and MCF-7/dox cell lines Downregulation of P-gp expression
EGFR↓, MCF-7 and MDA-MB-231 cells Suppressed EGFR signaling and inhibited PI3K/Akt/mTOR/GSK-3β
GSK‐3β↓,
mTOR↓,
RAGE↓, IA Paca-2, BxPC3, AsPC-1, HPAC and PANC1 Silencing RAGE expression
HSP27↓, Breast cancer In vivo NOD/SCID mice Inhibited the overexpression of Hsp27
VEGF↓, QC significantly reversed an elevation in profibrotic markers (VEGF, IL-6, TGF, COL-1, and COL-3)
TGF-β↓,
COL1↓,
COL3A1↓,
Showing Research Papers: 1 to 4 of 4
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
GSH↓, 1, HO-1↑, 1, ROS↑, 1,
Mitochondria & Bioenergetics ⓘ
MMP↓, 1, MMP∅, 1, XIAP↓, 1,
Core Metabolism/Glycolysis ⓘ
cMyc↓, 1,
Cell Death ⓘ
Akt↓, 1, Apoptosis↑, 1, BAX↑, 1, Bcl-2↓, 1, Casp10↑, 1, Casp3↑, 1, Casp8↑, 1, Casp9↑, 1, DR5↑, 1, Fas↑, 1, iNOS↓, 1, survivin↓, 1, TNFR 1↑, 1, TRAILR↑, 1,
Kinase & Signal Transduction ⓘ
Sp1/3/4↓, 1,
Transcription & Epigenetics ⓘ
other↓, 1,
Protein Folding & ER Stress ⓘ
HSP27↓, 1,
DNA Damage & Repair ⓘ
DFF45↑, 1, P53↑, 1, cl‑PARP↑, 1,
Cell Cycle & Senescence ⓘ
cycD1/CCND1↓, 1, TumCCA↑, 2,
Proliferation, Differentiation & Cell State ⓘ
CSCs↓, 1, EMT↓, 1, GSK‐3β↓, 1, mTOR↓, 1, NOTCH1↓, 1, PI3K↓, 1, STAT3↓, 1,
Migration ⓘ
Ca+2↝, 1, COL1↓, 1, COL1A1↓, 1, COL3A1↓, 2, E-cadherin↓, 1, LEF1↓, 1, MMP2↓, 2, MMP7↓, 1, MMP9↓, 1, MMPs↓, 1, RAGE↓, 1, Slug↓, 1, Snail↓, 1, TGF-β↓, 1, TIMP1↓, 1, TSP-1↑, 1, TumCMig↓, 1, TumCP↓, 1, Vim↓, 1, α-SMA↓, 1, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, EGFR↓, 1, VEGF↓, 1,
Barriers & Transport ⓘ
P-gp↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IFN-γ↓, 1, IKKα↓, 1, IL6↓, 1, IL8↓, 1, Inflam↓, 1, NF-kB↓, 1, TNF-α↓, 1,
Drug Metabolism & Resistance ⓘ
P450↓, 1,
Clinical Biomarkers ⓘ
EGFR↓, 1, IL6↓, 1, RAGE↓, 1,
Total Targets: 73
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, GSH↑, 2, MDA↓, 1, NRF2↑, 1, ROS↓, 3,
Core Metabolism/Glycolysis ⓘ
ALAT↓, 1,
Proliferation, Differentiation & Cell State ⓘ
EMT↓, 1,
Migration ⓘ
COL1↓, 1, COL3A1↓, 2, E-cadherin↑, 1, Fibronectin↓, 1, MMP2↓, 1, Smad7↑, 1, TGF-β↓, 1, Vim↓, 1, α-SMA↓, 3,
Clinical Biomarkers ⓘ
ALAT↓, 1, ALP↓, 1, AST↓, 1,
Functional Outcomes ⓘ
hepatoP↑, 2,
Total Targets: 20
Scientific Paper Hit Count for: COL3A1, collagen3a
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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