Zhou Ping, Hu Jian, Wang Xiaoqin, Wang Jingyuan, Zhang Yong, Wang Cong
Clinical Laboratory, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.
Chest Surgery, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.
Oncol Lett. 2018 Apr;15(4):5201-5207. doi: 10.3892/ol.2018.7961. Epub 2018 Feb 6.
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.
本研究评估了表皮生长因子受体（EGFR）及其分子靶点在非小细胞肺癌中的功能。本研究结果表明，与肺癌组织样本相比，正常相邻组织标本中EGFR蛋白和mRNA表达降低。与BEAS-2B正常支气管上皮细胞相比，SW-900和A549肺癌细胞中EGFR和磷酸化（p）-细胞外信号调节激酶（ERK）蛋白表达增加，且与BEAS-2B细胞相比，SW-900和A549细胞中微小RNA（miR）200a表达受到抑制。与BEAS-2B细胞相比，下调miR200a表达显著抑制A549细胞的增殖并促进其凋亡以及半胱天冬酶（CASP）3和CASP9功能，且显著抑制A549细胞中EGFR和p-ERK蛋白表达。本研究结果表明，下调miR200a可通过调节EGFR和ERK 1/2信号通路显著抑制A549细胞的增殖并促进其凋亡。
