Epidermal growth factor receptor expression affects proliferation and apoptosis in non-small cell lung cancer cells via the extracellular signal-regulated kinase/microRNA 200a signaling pathway.

Abstract

The present study assessed the function of epidermal growth factor receptor (EGFR) and its molecular targets in non-small cell lung cancer. The results of the present study demonstrated that EGFR protein and mRNA expression in the normal adjacent tissue specimens was decreased compared with that in the lung cancer tissue samples. Compared with the BEAS-2B normal bronchial epithelial cells, EGFR and phosphorylated (p)-extracellular signal-regulated kinase (ERK) protein expression in the SW-900 and A549 lung cancer cells was increased and microRNA (miR)200a expression in the SW-900 and A549 cells was inhibited compared with the BEAS-2B cells. Downregulating miR200a expression significantly suppressed proliferation and promoted apoptosis and caspase (CASP)3 and CASP9 function in the A549 cells and significantly inhibited EGFR and p-ERK protein expression in the A549 cells, compared with the BEAS-2B cells. The results of the present study indicated that downregulating miR200a significantly suppressed proliferation and promoted apoptosis in A549 cells via the regulation of the EGFR and ERK 1/2 signaling pathways.