Study On C-jun Mediated By EGFR Regulating Cyclin D1and Cyclin E Effect On Proliferation Of Nsclc Cells

Objective:Lung cancer is one of the most common malignant tumors. Studies have shown that epidermal growth factor receptor (EGFR) is often overexpressed in non-small-cell lung cancer(NSCLC).EGFR overexpression and EGFR-mediated signal transduction pathways is closely related to the development of NSCLC. This study aims to investigate the mechanism of EGFR signaling pathway on cell proliferation of lung adenocarcinoma SPC-A-1cells.Method:SPC-A-1cells were transfected with small interfering RNA (siRNA). The expression levels of proteins were detected by Westernblotting after siRNA-mediated knockdown. Cell proliferation assay and colony formation assay were used to examine the capability of cell proliferation. The growth curve was used to observe the cell growth.Result:EGFR siRNA transfecting SPC-A-1cells, the expression levels of EGFR and downstream signaling molecules (c-Jun, Cyclin D1, and Cyclin E) were decreased remarkably. c-Jun siRNA transfecting SPC-A-1cells, the expression levels of c-Jun and downstream signaling molecules (Cyclin D1and Cyclin E) were decreased remarkably. Further experiments showed, after siRNA-mediated knockdown EGFR, the capability of cell proliferation decreased remarkably, and the cloning efficiency were decreased remarkably (P<0.05), then the cell growth was inhibited significantly. Moreover, after siRNA-mediated knockdown c-Jun, the capability of cell proliferation decreased remarkably, and the cloning efficiency were decreased remarkably(P <0.05), then cell growth was inhibited significantly.Conclusion:EGFR might mediate c-Jun regulating the expression of Cyclin Dl and Cyclin E, which may play a key role on the proliferation of lung cancer cells.