COL1 Cancer Research Results

COL1, Collagen I: Click to Expand ⟱
Source:
Type:
Collagen I, primarily composed of two chains encoded by the genes COL1A1 and COL1A2.
- Collagen I is the most abundant collagen in the human body and is a major component of the extracellular matrix (ECM), providing structural support to tissues.
- It is typically a heterotrimer composed of two α1(I) chains (COL1A1) and one α2(I) chain (COL1A2).

- Cancer progression is often accompanied by significant remodeling of the ECM.
- Collagen I deposition frequently increases in many solid tumors, contributing to a dense and fibrotic stroma (desmoplasia).
- Increased collagen I deposition can lead to higher ECM stiffness, which in turn modifies cell signaling and behavior.

Expression Patterns:
- Tumors such as breast, pancreatic, colorectal, and lung cancers often exhibit elevated levels of collagen I.
- High collagen I expression or deposition in the tumor stroma is frequently correlated with a more aggressive tumor phenotype.
Scientific Papers found: Click to Expand⟱
2662- AL,    Allicin inhibits tubular epithelial-myofibroblast transdifferentiation under high glucose conditions in vitro
- in-vitro, Nor, HK-2
*α-SMA↓, Allicin partially reversed the high-glucose-induced increase in α-SMA, vimentin and collagen I expression (P<0.01 at 20 µg/ml), increased the expression of E-cadherin
*Vim↓,
*COL1↓,
*E-cadherin↑,
*TGF-β1↓, and significantly downregulated the high glucose-induced expression of TGF-β1 and p-ERK1/2 in a dose-dependent manner (P<0.05).
*p‑ERK↓,
*EMT↓, suggested that high glucose concentrations induced the EMT of HK-2 cells, and that allicin was able to inhibit the EMT, potentially via regulation of the ERK1/2-TGF-β1 signaling pathway.

1104- CAR,    Carvacrol Ameliorates Transforming Growth Factor-β1-Induced Extracellular Matrix Deposition and Reduces Epithelial-Mesenchymal Transition by Regulating The Phosphatidylinositol 3-Kinase/Protein Kinase B Pathway In Hk-2 Cells
- in-vitro, Kidney, HK-2
tumCV↓,
COL4↓,
COL1↓,
Fibronectin↓,
E-cadherin↑, attenuated (TGF-β1-induced) decrease of E-cadherin
Snail↑,
Vim↑,
α-SMA↑,
PI3K↓,
Akt↓,

1117- Gb,    Ginkgobiloba leaf extract mitigates cisplatin-induced chronic renal interstitial fibrosis by inhibiting the epithelial-mesenchymal transition of renal tubular epithelial cells mediated by the Smad3/TGF-β1 and Smad3/p38 MAPK pathways
- vitro+vivo, Kidney, HK-2
α-SMA↓,
COL1↓,
TGF-β↓, TGF-β1
SMAD2↓,
SMAD3↓,
p‑SMAD2↓,
p‑SMAD3↓, EGb inhibited cisplatin-induced EMT of renal tubular epithelial cells by downregulating the smad3/TGF-β1 and smad3/p38 MAPK pathways and ultimately effectively ameliorated CRIF.
p38↓,
p‑p38↓,
Vim↓,
TIMP1↓,
CTGF↓,
E-cadherin↑,
MMP1:TIMP1↑,

1257- PI,    Piperlongumine attenuates bile duct ligation-induced liver fibrosis in mice via inhibition of TGF-β1/Smad and EMT pathways
- ex-vivo, LiverDam, NA
*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↓,

923- QC,    Quercetin as an innovative therapeutic tool for cancer chemoprevention: Molecular mechanisms and implications in human health
- Review, Var, NA
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 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 1,   HO-1↑, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp10↑, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   DR5↑, 1,   Fas↑, 1,   iNOS↓, 1,   p38↓, 1,   p‑p38↓, 1,   survivin↓, 1,   TNFR 1↑, 1,   TRAILR↑, 1,  

Kinase & Signal Transduction ⓘ

Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

other↓, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

HSP27↓, 1,  

DNA Damage & Repair ⓘ

DFF45↑, 1,   P53↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   EMT↓, 1,   GSK‐3β↓, 1,   mTOR↓, 1,   NOTCH1↓, 1,   PI3K↓, 2,   STAT3↓, 1,  

Migration ⓘ

Ca+2↝, 1,   COL1↓, 3,   COL3A1↓, 1,   COL4↓, 1,   CTGF↓, 1,   E-cadherin↓, 1,   E-cadherin↑, 2,   Fibronectin↓, 1,   LEF1↓, 1,   MMP1:TIMP1↑, 1,   MMP2↓, 1,   MMP7↓, 1,   MMPs↓, 1,   RAGE↓, 1,   Slug↓, 1,   SMAD2↓, 1,   p‑SMAD2↓, 1,   SMAD3↓, 1,   p‑SMAD3↓, 1,   Snail↓, 1,   Snail↑, 1,   TGF-β↓, 2,   TIMP1↓, 1,   TSP-1↑, 1,   Vim↓, 2,   Vim↑, 1,   α-SMA↓, 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: 83

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   GSH↑, 1,   NRF2↑, 1,   ROS↓, 2,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 2,   p‑ERK↓, 1,  

Migration ⓘ

COL1↓, 2,   COL3A1↓, 1,   E-cadherin↑, 2,   Fibronectin↓, 1,   MMP2↓, 1,   Smad7↑, 1,   TGF-β↓, 1,   TGF-β1↓, 1,   Vim↓, 2,   α-SMA↓, 3,  

Functional Outcomes ⓘ

hepatoP↑, 1,  
Total Targets: 17

Scientific Paper Hit Count for: COL1, Collagen I
1 Allicin (mainly Garlic)
1 Carvacrol
1 Ginkgo biloba
1 Piperine
1 Quercetin
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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