Reduced expression of fibroblast growth factor receptor 2IIIb in hepatocellular carcinoma induces a more aggressive growth.

摘要: Fibroblast growth factor receptor 2 isoform b (FGFR2-IIIb) is highly expressed in hepatocytes and plays an important role liver homeostasis regeneration. Here, we analyzed the expression function of FGFR2-IIIb hepatocellular carcinoma (HCC). HCC tissues cell lines was lower than primary human nontumorous tissue. FGFR2-IIIb-negative HCCs showed a significantly higher Ki-67 labeling index, loss correlated with vascular invasion more advanced tumor stages. A decrease FGFR-2IIIb not related to promoter hypermethylation. However, PCR analysis indicated that chromosomal deletion at 10q accounted for FGFR2 subset cells. re-expression stable transfected induced basal apoptosis rate reduced proliferation migratory potential vitro. In nude mice, re-expressing cells grew slower, terminal deoxynucleotidyl transferase-mediated dUTP nick-end assay revealed rates. The antitumorigenic effects were affected by keratinocyte or inhibitor FGFR-phosphorylation, indicating they are independent tyrosine kinase activation. conclusion, our data indicate inhibits tumorigenicity Identification molecular mechanisms promoting regeneration normal tissue while suppressing malignancy may lead novel therapeutic targets this aggressive tumor.