ArticleWorld journal of gastroenterology2005
Focal adhesion kinase and Src phosphorylations in HGF-induced proliferation and invasion of human cholangiocarcinoma cell line, HuCCA-1.
Article in World journal of gastroenterology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- Tiliacorinine as a Promising Candidate for Cholangiocarcinoma Therapy via Oxidative Stress Molecule Modulation: A Study Integrating Network Pharmacology, Molecular Docking and Molecular Dynamics Simulation.Antioxidants (Basel, Switzerland) · 2025Article
- Spatial Transcriptomics Analysis: Maternal Obesity Impairs Myogenic Cell Migration and Differentiation during Embryonic Limb Development.International journal of molecular sciences · 2024Article
- Suppressing of Src-Hic-5-JNK-AKT Signaling Reduced GAPDH Expression for Preventing the Progression of HuCCT1 Cholangiocarcinoma.Pharmaceutics · 2022Article
- Targeting Src-Hic-5 Signal Cascade for Preventing Migration of Cholangiocarcinoma Cell HuCCT1.Biomedicines · 2022Article
- Focal adhesion kinase (FAK) promotes cholangiocarcinoma development and progression via YAP activation.Journal of hepatology · 2021Article
- Loss of desmoglein-2 promotes gallbladder carcinoma progression and resistance to EGFR-targeted therapy through Src kinase activation.Cell death and differentiation · 2021Article
- High glucose enhances progression of cholangiocarcinoma cells via STAT3 activation.Scientific reports · 2016Article
- Deoxycholic Acid Could Induce Apoptosis and Trigger Gastric Carcinogenesis on Gastric Epithelial Cells by Quantitative Proteomic Analysis.Gastroenterology research and practice · 2016Article
- Src-signaling interference impairs the dissemination of blood-borne tumor cells.Cell and tissue research · 2012Article
- The role of cancer-associated myofibroblasts in intrahepatic cholangiocarcinoma.Nature reviews. Gastroenterology & hepatology · 2011Review
- CCR9 interactions support ovarian cancer cell survival and resistance to cisplatin-induced apoptosis in a PI3K-dependent and FAK-independent fashion.Journal of ovarian research · 2010Article
- Involvement of PI3K and ERK1/2 pathways in hepatocyte growth factor-induced cholangiocarcinoma cell invasion.World journal of gastroenterology · 2010Article
- Anti-metastatic Potential of Natural Triterpenoid Cucurbitacin B Against Cholangiocarcinoma Cells by Targeting Src Protein.Integrative cancer therapiesArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo study the role of focal adhesion kinase (FAK) and its association with Src in hepatocyte growth factor (HGF)-induced cell signaling in cholangiocarcinoma progression.
methodsPreviously isolated HuCCA-1 cells were re-characterized by immunofluorescent staining and reverse transcriptase-polymerase chain reaction assay for the expression of cytokeratin 19, HGF and c-Met mRNA. Cultured HuCCA-1 cells were treated with HGF and determined for cell proliferation and invasion effects by MTT and invasion assays. Western blotting, immunoprecipitation, and co-immunoprecipitation were also performed to study the phosphorylation and interaction of FAK and Src. A novel Src inhibitor (AZM555130) was applied in cultures to investigate the effects on FAK phosphorylation inhibition and on cell proliferation and invasion.
resultsHGF enhanced HuCCA-1 cell proliferation and invasion by mediating FAK and Src phosphorylations. FAK-Src interaction occurred in a time-dependent manner that Src was proved to be an upstream signaling molecule to FAK. The inhibitor to Src decreased FAK phosphorylation level in correlation with the reduction of cell proliferation and invasion.
conclusionFAK plays a significant role in signaling pathway of HGF-responsive cell line derived from cholangiocarcinoma. Autophosphorylated Src, induced by HGF, mediates Src kinase activation, which subsequently phosphorylates its substrate, FAK, and signals to cell proliferation and invasion.
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