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⟱
3516- Bor,    Boron in wound healing: a comprehensive investigation of its diverse mechanisms
- Review, Wounds, NA
*Inflam↓, anti-inflammatory, antimicrobial, antioxidant, and pro-proliferative effects.
*antiOx↑,
*ROS↓, The antioxidant properties of boron help protect cells from oxidative stress, a common feature of chronic wounds that can impair healing
*angioG↑, Boron compounds exhibit diverse therapeutic actions in wound healing, including antimicrobial effects, inflammation modulation, oxidative stress reduction, angiogenesis induction, and anti-fibrotic properties.
*COL1↑, Boron has been shown to increase the expression of proteins involved in wound contraction and matrix remodeling, such as collagen, alpha-smooth muscle actin, and transforming growth factor-beta1.
*α-SMA↑,
*TGF-β↑,
*BMD↑, Animals treated with boron showed favorable changes in bone density, wound healing, embryonic development, and liver metabolism
*hepatoP↑,
*TNF-α↑, BA elevates TNF-α and heat-shock proteins 70 that are related to wound healing.
*HSP70/HSPA5↑,
*SOD↑, antioxidant properties of BA showed that boron protects renal tissue from I/R injury via increasing SOD, CAT, and GSH and decreasing MDA and total oxidant status (TOS)
*Catalase↑,
*GSH↑,
*MDA↓,
*TOS↓,
*IL6↓, Boron supports gastric tissue by alleviating ROS, MDA, IL-6, TNF-α, and JAK2/STAT3 action, as well as improving AMPK activity
*JAK2↓,
*STAT3↓,
*AMPK↑,
*lipid-P↓, boron may improve wound healing by hindering lipid peroxidation and increasing the level of VEGF
*VEGF↑,
*Half-Life↝, Boron is a trace element, usually found at a concentration of 0–0.2 mg/dL in plasma with a half-life of 5–10 h, and 1–2 mg of it is needed in the daily diet

8105- KAE,    Chemo-preventive and therapeutic effect of the dietary flavonoid kaempferol: A comprehensive review
- Review, Var, NA
Apoptosis↑, It induces apoptosis (HeLa cervical cancer cells), decreases cell viability (G2/M phase), downregulates phosphoinositide 3-kinase (PI3K)/AKT
tumCV↓,
TumCCA↑,
PI3K↓,
Akt↓,
EMT↓, suppresses protein expression of epithelial-mesenchymal transition (EMT)-related markers including N-cadherin, E-cadherin, Slug, and Snail, and metastasis-related markers such as matrix metallopeptidase 2 (MMP-2).
N-cadherin↓,
E-cadherin↓, nhibition of N‐cadherin, E‐cadherin, Slug, Snail, and MMP‐2, 9, and cathepsin B, D
Slug?,
Snail?,
MMP2↓,
MMP9↓,
CTSB↓,
CTSD↓,
Casp3↑, Activation of caspase signals such as caspase‐3, ‐8, and ‐9
Casp8↑,
Casp9↑,
TIMP2↓, Down‐regulation of phosphorylated TIMP2, AKT, and MMP2 levels
Akt↓,
TumCD↑, Induction of cell apoptotic cell death, intracellular free calcium elevation, and mitochondrial membrane potential disruption.
i-Ca+2↑,
MMP↓,
*ROS↓, Enhances the concentrations of superoxide dismutase, catalase, glutathione peroxidase, and glutathione‐S‐transferase.
*SOD↑,
*Catalase↑,
*GPx↑,
*GSTs↑,
*AST↓, Lowers aspartate aminotransferase, alanine aminotransferase, malondialdehyde (MDA).
*ALAT↓,
*MDA↓,
*CYP2E1↓, Decreases activity of hepatic microsomal enzyme cytochrome 2E1 (CYP2E1) expression
*NRF2↑, Increases mRNA and protein expression of Nrf2‐regulated genes
*AGEs↓, Suppresses advanced glycation end products (AGEs)‐ receptor.
*IL6↓, Reduces levels of IL‐6, TNF‐α, and NF‐κB.
*TNF-α↓,
*NF-kB↓,
*Casp3↓, Lowers expressions of Caspase‐3 and Bax,
*BAX↓,
*antiAll↑, Antiallergic Inhibits COX2‐mediated production of prostaglandin D2 and prostaglandin F2α.
*COX2/PTGS2↓,
*PGE2↓,
*RUNX2↑, Increases expression of the osteoblast‐activated factors RUNX‐2, BMP‐2, osterix, collagen I, and SQSTM1/p62
*BMP2↑,
*COL1↑,
*p62↑,
*FASN↓, Reduces expressions of lipin1, FASN, LPAATθ (lysophosphatidic acid acyltransferase), SREBP‐1C (fatty acid synthetic proteins), and DGAT1 (triglyceride synthetic enzymes).
*DGAT1↓,
FOXP3↑, kaempferol significantly enhanced the inhibitory effect of proliferation, increased the FOXP3 expression level,
DNAdam↑, s induction of DNA damage, enhancement DNA condensation
ROS↑, anti‐cancer property is mainly defined by ROS accumulation due to catalase inhibition as depicted in Figure 2
Catalase↓,
*ROS↓, (A/R)‐induced injury of cardiomyocytes by increasing cell viability, lowering LDH release, reducing A/R‐induced ROS generation, loss of Δψm, and release of cytochrome c from mitochondria into cytosol.
*MMP↑,
*Cyt‑c↓,


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↓, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 2,   Apoptosis↑, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   TumCD↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

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

CTSB↓, 1,   CTSD↓, 1,   EMT↓, 1,   PI3K↓, 1,  

Migration(tgid=13) ⓘ

i-Ca+2↑, 1,   E-cadherin↓, 1,   MMP2↓, 1,   MMP9↓, 1,   N-cadherin↓, 1,   Slug?, 1,   Snail?, 1,   TIMP2↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

FOXP3↑, 1,  
Total Targets: 25

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

antiAll↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Catalase↑, 2,   CYP2E1↓, 1,   GPx↑, 1,   GSH↑, 1,   GSTs↑, 1,   lipid-P↓, 1,   MDA↓, 2,   NRF2↑, 1,   ROS↓, 3,   SOD↑, 2,   TOS↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   AMPK↑, 1,   DGAT1↓, 1,   FASN↓, 1,  

Cell Death(tgid=5) ⓘ

BAX↓, 1,   BMP2↑, 1,   Casp3↓, 1,   Cyt‑c↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

HSP70/HSPA5↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

p62↑, 1,  

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

RUNX2↑, 1,   STAT3↓, 1,  

Migration(tgid=13) ⓘ

COL1↑, 2,   TGF-β↑, 1,   α-SMA↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↑, 1,   VEGF↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IL6↓, 2,   Inflam↓, 1,   JAK2↓, 1,   NF-kB↓, 1,   PGE2↓, 1,   TNF-α↓, 1,   TNF-α↑, 1,  

Protein Aggregation(tgid=19) ⓘ

AGEs↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Half-Life↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   BMD↑, 1,   IL6↓, 2,  

Functional Outcomes(tgid=23) ⓘ

hepatoP↑, 1,  
Total Targets: 46

Scientific Paper Hit Count for: COL1, Collagen I
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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