SOCS3 expression is inversely correlated with Pyk2 in non-small cell lung cancer and exogenous SOCS3 inhibits proliferation and invasion of A549 cells

SummaryAimsWe have confirmed that suppressor of cytokine signalling 3 (SOCS3) is silenced and proline-rich tyrosine kinase 2 (Pyk2) is over-expressed in non-small cell lung cancer (NSCLC). The aim of this study was to investigate the correlation of SOCS3 and Pyk2 expression in NSCLC, and the effects of SOCS3 up-regulation on A549 cells.MethodsOne hundred cases of NSCLC were detected for the expression of SOCS3 and Pyk2 by immunohistochemistry. The expression of SOCS3 and Pyk2 were also examined in human bronchial epithelial cells (HBE) and six lung cancer cell lines using Western blot and immunofluorescence staining. Then plasmid containing full-length SOCS3 was transfected into A549 cells to further investigate the effects of SOCS3 over-expression on proliferation, apoptosis and invasion of transfected cells, which were examined using MTT flow cytometry and Transwell assays.ResultsOur results showed a significant negative correlation between SOCS3 and Pyk2 in both NSCLC tissues and cell lines. Up-regulation of SOCS3 increased the apoptotic rates of transfected cells, while the numbers of proliferative and invasive cells were decreased.ConclusionsOur data indicate that SOCS3 definitely plays roles in regulating Pyk2 expression, and up-regulation of SOCS3 could be an effective way to prevent the progression of NSCLC.