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↓,

7012- Fuc,    Fucoidan: A promising natural therapeutic agent for protecting human kidney health
- Review, EC, NA
*RenoP↑, Fucoidan exhibits significant anti-inflammatory effects in kidney protection.
*Inflam↓,
*antiOx↑, Antioxidant properties effectively reduce oxidative stress in renal tissues.
*ROS↓,
*BloodF↑, Enhances renal function by improving blood flow and diuresis.
*diuretic↑,
*BioAv↓, High-MW fucoidans often display stronger anticoagulant and viscosity-modulating effects. However, they may have limited oral bioavailability,
*BioAv↑, whereas low- to medium-MW fractions show improved tissue penetration, more favorable absorption, and can retain potent anti-inflammatory and anti-fibrotic activities, making them attractive for chronic kidney disease applications
*MAPK↓, (LMWF) has been reported in models of renal ischemia-reperfusion injury, where it inhibits the MAPK signaling pathway and subsequently reduces inflammation and fibrosis
*ERK↑, fucoidan can activate the ERK/MAPK signaling pathway, which plays a crucial role in preserving the endothelial glycocalyx in CKD
*NLRP3↓, fucoidan attenuates NLRP3 inflammasome activation and subsequent podocyte pyroptosis, ultimately leading to improved renal function and reduced inflammation in diabetic kidney disease (DKD)
*NRF2↑, By inhibiting ROS-generating systems (e.g., NADPH oxidase) and activating Nrf2-dependent transcription of antioxidant genes, fucoidan limits mitochondrial dysfunction and prevents oxidative injury to podocytes and tubular epithelial cells
*MDA↓, fucoidan nanoparticles significantly reduced levels of malondialdehyde (MDA), a marker of lipid peroxidation and oxidative stress, while simultaneously upregulating the levels of superoxide dismutase (SOD) and glutathione peroxidase (GPx)
*SOD↑,
*GPx↑,
*Catalase↑, Altogether, fucoidan directly reduces renal oxidative stress by scavenging reactive oxygen species and upregulating endogenous antioxidant defenses (e.g., SOD, CAT, GPx) in tubular and glomerular cells, by suppressing upstream ROS generation
*lipid-P↓, fucoidan limits lipid peroxidation and DNA damage, thereby preserving podocyte integrity and tubular epithelial viability
*DNAdam↓,
*Fibrosis↓, Inhibition of fibrosis
*JAK2↓, fucoidan combats renal fibrosis is via the restriction of the JAK2/STAT3 signaling pathway.
*STAT3↓,
*uricA↓, By reducing serum uric acid levels, fucoidan significantly inhibits the activation of JAK2/STAT3, consequently decreasing the expression of key fibrotic markers such as collagen I and α-smooth muscle actin (α-SMA)
*COL1↓,
*α-SMA↓,
*SIRT1↑, fucoidan’s anti-fibrotic effects are further attributed to its activation of protective pathways such as Sirt-1, GLP-1R, and Nrf2/HO-1(
*HO-1↑,
*GLP-1R↑,
*HMGB1↓, Stimulating these protective pathways results in the inhibition of pro-fibrotic signaling cascades, including the HMGB1/RAGE/NF-κB/TGF-β1 pathway
*RAGE↓,
*NF-kB↓,
*TGF-β1↓,
*PI3K↓, Fucoidan also exhibits potential in curtailing the inflammatory processes associated with renal fibrosis through its inhibitory effects on the PI3K/Akt/NF-κB signaling cascade.
*Akt↓,
*GutMicro↑, research has elucidated the important role of gut microbiota in mediating the protective effects of fucoidan, suggesting that modulation of microbial communities may underlie its benefits in renal health
*SCFAs↑, Fucoidan’s positive impact on gut microbiota includes enhancing the production of short-chain fatty acids (SCFAs), especially butyrate, which are known to support gut integrity and overall health (
*Buty↑,
*IBI↑, Fucoidan's ability to enhance SCFA production has been linked to improved intestinal barrier integrity, a crucial factor in preventing the translocation of harmful substances into the bloodstream, which can exacerbate kidney injury
*TJ↑, Studies indicate that fucoidan can upregulate the expression of tight junction proteins, crucial for maintaining the integrity of the intestinal epithelium
*Dose↝, national approval in China for renal indications, indicate that fucoidan is generally safe at oral doses of 50–300 mg/day and up to 1–3 g/day in short‑ to mid‑term studies, with no major hematologic, hepatic, or renal toxicity reported.

1117- GBE,    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↓,
CCN2/CTGF↓,
E-cadherin↑,
MMP1:TIMP1↑,

7492- H2,  Chemo,    Molecular Hydrogen Protects against Various Tissue Injuries from Side Effects of Anticancer Drugs by Reducing Oxidative Stress and Inflammation
- Review, Var, NA
*ROS↓, reduces reactive oxygen species, which have very strong oxidative capacity, and indirectly exerts antioxidant, anti-inflammatory
*antiOx↑,
*Inflam↓,
*chemoP↑, Our comprehensive literature review revealed that H2 protects against tissue injuries induced by cisplatin, oxaliplatin, doxorubicin, bleomycin, and gefitinib.
AntiCan↑, Animal and clinical studies showed that H2 itself exhibits anticancer activity, and its combination with anticancer drugs achieved excellent anticancer activity
ChemoSen↑,
chemoP↑, Our literature review revealed that H2 reduced the side effects of CIS-induced nephrotoxicity, ototoxicity, and ovarian injury, CIS- or OXA-induced peripheral neuropathy, DXR-induced cardiotoxicity and hepatotoxicity, and BLM- or GEF-induced lung inj
*BUN↓, CIS Nephrotoxicity BUN ↓, Creatinine ↓, TUNEL ↓
*creat↓,
*TUNEL↓,
*MDA↓, CIS Ototoxicity MDA ↓, 8-iso-PGF2α ↓
*SOD↑, CIS Ovarian injury SOD ↑, CAT ↑, MDA ↓, Nrf2 ↑
*Catalase↑,
*NRF2↑,
*BNP↓, DXR Cardiotoxicity and hepatotoxicity BNP ↓, AST ↓, ALT ↓, ROS ↓, MDA ↓, TNF-α ↓, IL-1β ↓, IL-6 ↓, TUNEL ↓, Bax/Bcl-2 ↓, Caspase-3 ↓, Caspase-8 ↓
*AST↓,
*ALAT↓,
*TNF-α↓,
*IL1β↓,
*IL6↓,
*Casp3↓,
*Casp9↓,
*GPx↑, BLM Lung injury ROS ↓, MDA ↓ TGF-β1 ↓,TNF-α ↓, GSH-PX ↑, E-cadherin ↑, Vimentin ↓, α-SMA ↓, Collagen I ↓
*E-cadherin↑,
*Vim↓,
*α-SMA↓,
*COL1↓,
*cardioP↑, H2 ameliorated DXR-induced cardiotoxicity and hepatotoxicity by attenuating inflammation and apoptosis.
*hepatoP↑,
*p‑mTOR↓, decreased the phosphorylated mammalian target of rapamycin (p-mTOR) to mTOR
*EMT↓, H2 gas also inhibited BLM-mediated epithelial-to-mesenchymal transition by increasing the expression level of the epithelial cell marker E-cadherin and decreasing that of the mesenchymal cell marker vimentin [
eff∅, On the other hand, H2 did not impair the anticancer effects of GEF in in vitro experiments on lung cancer cell lines or in in vivo experiments on carcinoma-bearing mice
*LPS↓, figure 2
*TLR4↓,
radioP↑, radioprotective effects of H2 have also been reported in many in vitro and in vivo studies, and clinical trials recently showed that the inhalation of H2 gas mitigated decreases in quality of life and bone marrow damage associated with radiation [

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/PTGS2↓,
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/ABCB1↓, 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 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

GSH↓, 1,   HO-1↑, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

cMyc↓, 1,  

Cell Death(tgid=5) ⓘ

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(tgid=6) ⓘ

Sp1/3/4↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↓, 1,   tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

HSP27↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

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

Cell Cycle & Senescence(tgid=11) ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

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

Migration(tgid=13) ⓘ

Ca+2↝, 1,   CCN2/CTGF↓, 1,   COL1↓, 3,   COL3A1↓, 1,   COL4↓, 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(tgid=14) ⓘ

angioG↓, 1,   EGFR↓, 1,   VEGF↓, 1,  

Barriers & Transport(tgid=15) ⓘ

P-gp/ABCB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IFN-γ↓, 1,   IKKα↓, 1,   IL6↓, 1,   IL8↓, 1,   Inflam↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   eff∅, 1,   P450↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EGFR↓, 1,   IL6↓, 1,   RAGE↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   chemoP↑, 1,   radioP↑, 1,  
Total Targets: 88

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

Buty↑, 1,   diuretic↑, 1,   GLP-1R↑, 1,   SCFAs↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 3,   Catalase↑, 2,   GPx↑, 2,   GSH↑, 1,   HO-1↑, 1,   lipid-P↓, 1,   MDA↓, 2,   NRF2↑, 3,   ROS↓, 4,   SOD↑, 2,   uricA↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   BUN↓, 1,   SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Casp3↓, 1,   Casp9↓, 1,   MAPK↓, 1,   TUNEL↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

EMT↓, 3,   ERK↑, 1,   p‑ERK↓, 1,   p‑mTOR↓, 1,   PI3K↓, 1,   STAT3↓, 1,  

Migration(tgid=13) ⓘ

COL1↓, 4,   COL3A1↓, 1,   E-cadherin↑, 3,   Fibronectin↓, 1,   Fibrosis↓, 1,   MMP2↓, 1,   RAGE↓, 1,   Smad7↑, 1,   TGF-β↓, 1,   TGF-β1↓, 2,   TJ↑, 1,   Vim↓, 3,   α-SMA↓, 5,  

Barriers & Transport(tgid=15) ⓘ

IBI↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

HMGB1↓, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 2,   JAK2↓, 1,   LPS↓, 1,   NF-kB↓, 1,   TLR4↓, 1,   TNF-α↓, 1,  

Protein Aggregation(tgid=19) ⓘ

NLRP3↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

BNP↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 1,   Dose↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   BloodF↑, 1,   creat↓, 1,   GutMicro↑, 1,   IL6↓, 1,   RAGE↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 1,   chemoP↑, 1,   hepatoP↑, 2,   RenoP↑, 1,  
Total Targets: 69

Scientific Paper Hit Count for: COL1, Collagen I
1 Allicin (mainly Garlic)
1 Carvacrol
1 Fucoidan
1 Ginkgo biloba
1 Hydrogen Gas
1 Chemotherapy
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

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:1004  State#:%  Dir#:1
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