CCN2/CTGF Cancer Research Results

CCN2/CTGF, Connective Tissue Growth Factor: Click to Expand ⟱
Source:
Type: prognostic biomarker
CTGF is a matricellular protein that belongs to the CCN (Cyr61/CTGF/Nov) family. It plays a pivotal role in diverse biological processes, including cell adhesion, migration, proliferation, and differentiation. CTGF is also involved in wound healing and fibrosis. In cancer, CTGF’s function is multifaceted, affecting tumor growth, angiogenesis, and the remodeling of the tumor microenvironment.

CTGF is overexpressed in several cancer types, such as pancreatic, breast, and prostate cancers. In these contexts, higher levels of CTGF have been associated with enhanced tumor growth, angiogenesis, and metastasis.

Elevated CTGF expression often correlates with adverse clinical features.

CCN2 - Cellular Communication Network Factor 2 / Connective Tissue Growth Factor

Abbreviation: CCN2, CTGF

Type: Matricellular protein / extracellular signaling protein

Function: CCN2 is a secreted matricellular protein that regulates cell adhesion, migration, proliferation, extracellular-matrix remodeling, fibrosis, angiogenesis, and interactions between tumor cells and stromal cells. It is strongly influenced by signaling pathways including TGF-β, YAP/TAZ, integrins, and growth-factor signaling.

Cancer: ↑ Frequently increased in tumors and tumor-associated stroma. Elevated CCN2 can promote fibrosis, cancer-associated fibroblast activation, extracellular-matrix deposition, tumor-cell survival, invasion, angiogenesis, metastatic niche formation, and resistance to therapy. Its effects are context-dependent, but increased CCN2 is predominantly associated with tumor progression in many solid cancers.
Scientific Papers found: Click to Expand⟱
7907- Api,  IVT,    Anticancer Potential of Apigenin and Isovitexin with Focus on Oncogenic Metabolism in Cancer Stem Cells
- Review, Var, NA
ChemoSen↑, Two natural flavonoids, apigenin and isovitexin, have been shown to act synergistically with conventional chemotherapeutic drugs by sensitizing CSCs, ultimately leading to improved therapeutic efficacy.
CSCs↓,
Wnt↓, suppression of the Wnt/β-catenin signaling pathway, the inhibition of nuclear factor-κB protein expression, and the downregulation of the cell cycle via upregulation of p21 and cyclin-dependent kinases
β-catenin/ZEB1↓,
PI3K↓, Figure 3
MMP↓,
TumMeta↓,
MAPK↓,
VEGF↓,
MMP9↓,
TGF-β↓,
Inflam↓,
COX2/PTGS2↓,
IL6↓,
NF-kB↓,
TumCCA↑,
P53↑,
cycD1/CCND1↓,
BAX↑,
Casp↓,
Bcl-2↓,
CD133↓, Brain U87MG and U373MG Apigenin 25–50 μM for 2–21 days ↓Self-renewal capacity, ↓cell growth, ↓clonogenicity, ↓invasiveness ↓CD133, ↓NANOG, ↓SOX2, ↓c-Met, ↓Akt
Nanog↓,
SOX2↓,
Akt↓,
TumCP↓, Breast MDA-MB-231 and MDA-MB-436 Apigenin 2–64 μM for 48 h ↓Proliferation, ↓migration, ↓stemness features, ↓mammospheres, ↓self-renewal capability ↓YAP/TAZ activity, ↓CTGF, ↓CYR61, ↓YAP/TAZ-TEADs
TumCMig↓,
YAP/TEAD↓,
CCN2/CTGF↓,
CCN1/CYR61↓,
SIRT3↓, Breast TNBCs Apigenin 12.5–200 µg/µL for 24 h ↓Stemness properties, ↓mammosphere formation, ↓clonogenic potential ↓SIRT3, ↓SIRT6
SIRT6↓,
PCNA↓, Osteosarcoma U2OS-SC tumors in nude mice Isovitexin 10–40 mg/kg for 2 weeks ↓Tumor growth, ↓tumor size ↓CD133, ↓PCNA, ↓Bcl-2, ↓ DNMT1, ↑apoptotic index, ↑miR-34a
DNMT1↓,
miR-34a↑,

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↑,

7365- HibSad,    Insight into the molecular evidence supporting the remarkable chemotherapeutic potential of Hibiscus sabdariffa L
- Review, Var, NA
chemoPv↑, Both crude extracts and pure compounds of the plant were reported to induce chemoprevention, selective cytotoxicity, cell cycle arrest, apoptosis, autophagy and anti-metastasis effects in varied types of human cancer cells.
selectivity↑,
TumCCA↑,
Apoptosis↑,
TumAuto↑,
TumMeta↓,
ATG5↑, figure 3
Beclin-1↑,
LC3II↑,
MMP2↓,
MMP9↓,
CD31/PECAM-1↓,
VEGF↓,
uPA↓,
TIMP2↑,
NF-kB↓,
p38↑,
P53↑,
Casp3↑,
Casp8↑,
Casp9↑,
Bcl-2↓,
BAX↑,
Cyt‑c↑,
TNF-α↑,
Fas↑,
FasL↑,
JNK↑,
cJun↑,
angioG↓,
VEGFR2/KDR/Flk1↓,
PCNA↓,
CCN2/CTGF↓,
RAGE↓,

7701- IP6,    Inositol hexaphosphate sensitizes hepatocellular carcinoma to oxaliplatin relating inhibition of CCN2-LRP6-β-catenin-ABCG1 signaling pathway
- vitro+vivo, HCC, Hep3B - NA, NA, MHCC-97H
AntiCan↑, We proved that IP6 treatment exhibited independent anticancer effect and synergistic anti-proliferative effects in combination with oxaliplatin in HCC.
ChemoSen↑, ABCG1 was contributed to oxaliplatin resistance, and inhibition of ABCG1 were one of the mechanisms of IP6 treatment on HCC oxaliplatin resistance
LRP6↓, The IP6 treatment exhibited inhibition of CCN2-LRP6-Wnt/β-catenin signaling pathway and downregulation of ABCG1 in HCC cells.
Wnt↓,
β-catenin/ZEB1↓,
CCN2/CTGF↓,
ABCG1↓, The expression of ABCG1 and CCN2 in HCC cells was upregulated by oxaliplatin treatment and inhibited by IP6
TumCP↓, IP6 directly inhibited the ability of proliferation and migration in HCC
TumCMig↓,


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:


NA, unassigned(tgid=0) ⓘ

ABCG1↓, 1,   CCN1/CYR61↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

SIRT3↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 1,   BAX↑, 2,   Bcl-2↓, 2,   Casp↓, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   Fas↑, 1,   FasL↑, 1,   JNK↑, 1,   MAPK↓, 1,   p38↓, 1,   p38↑, 1,   p‑p38↓, 1,   YAP/TEAD↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

cJun↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   Beclin-1↑, 1,   LC3II↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNMT1↓, 1,   P53↑, 2,   PCNA↓, 2,   SIRT6↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 2,  

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

CD133↓, 1,   CSCs↓, 1,   LRP6↓, 1,   miR-34a↑, 1,   Nanog↓, 1,   PI3K↓, 1,   SOX2↓, 1,   Wnt↓, 2,  

Migration(tgid=13) ⓘ

CCN2/CTGF↓, 4,   CD31/PECAM-1↓, 1,   COL1↓, 1,   E-cadherin↑, 1,   MMP1:TIMP1↑, 1,   MMP2↓, 1,   MMP9↓, 2,   RAGE↓, 1,   SMAD2↓, 1,   p‑SMAD2↓, 1,   SMAD3↓, 1,   p‑SMAD3↓, 1,   TGF-β↓, 2,   TIMP1↓, 1,   TIMP2↑, 1,   TumCMig↓, 2,   TumCP↓, 2,   TumMeta↓, 2,   uPA↓, 1,   Vim↓, 1,   α-SMA↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   VEGF↓, 2,   VEGFR2/KDR/Flk1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

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

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 2,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,   RAGE↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   chemoPv↑, 1,  
Total Targets: 76

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: CCN2/CTGF, Connective Tissue Growth Factor
1 Apigenin (mainly Parsley)
1 Isovitexin
1 Ginkgo biloba
1 Hibiscus sabdariffa
1 IP6 (Inositol 1,2,3,4,5,6-hexakisphosphate)
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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