Zhang Hong-Bo, Sun Li-Chao, Ling Lan, Cong Lu-Hong, Lian Rui
Department of Emergency Medicine, China-Japan Friendship Hospital, Beijing 100029, P.R. China.
Exp Ther Med. 2016 Sep;12(3):1795-1802. doi: 10.3892/etm.2016.3555. Epub 2016 Jul 27.
MicroRNAs (miRs) regulate the proliferation and metastasis of numerous cancer cell types. It was previously reported that miR-143 levels were downregulated in non-small cell lung cancer (NSCLC) tissues and cell lines, and that the migration and invasion of NSCLC cells was inhibited upon suppression of cell proliferation and colony formation by the upregulation of miR-143. Epidermal growth factor receptor (EGFR), which is a vital factor in the promotion of cancer cell proliferation and has been investigated as a potential focus in cancer therapy, has been reported to be a possible target of miR-143. The present study aimed to investigate the role of miR-143 in NSCLC using NSCLC cell lines and primary cells from NSCLC patients. NSCLC cells were co-transfected with EGFR and miR-143, and the mRNA and protein expression of EGFR were analyzed. Furthermore, the activity of the transfected cancer cells with regard to colony formation, migration, invasion and apoptosis were evaluated. The levels of miR-143 were decreased in the NSCLC cell lines and primary cells from patients with NSCLC compared with the controls. Following transfection with miR-143, the ability of NSCLC cells to proliferate, form colonies, migrate and invade was inhibited. Similarly, knockdown of EGFR led to the suppression of NSCLC cell proliferation. The mRNA and protein expression levels of EGFR were significantly reduced following miR-143 overexpression, and the level of miR-143 was inversely correlated with that of EGFR in NSCLC cells. The results of the present study demonstrated that miR-143 was able to suppress NSCLC cell proliferation and invasion by inhibiting the effects of EGFR, suggesting that EGFR may be considered a potential target for NSCLC therapy.
微小RNA(miR)可调节多种癌细胞类型的增殖和转移。此前有报道称,非小细胞肺癌(NSCLC)组织和细胞系中miR-143水平下调,上调miR-143抑制细胞增殖和集落形成后,NSCLC细胞的迁移和侵袭也受到抑制。表皮生长因子受体(EGFR)是促进癌细胞增殖的关键因子,已被作为癌症治疗的潜在靶点进行研究,据报道它可能是miR-143的靶点。本研究旨在利用NSCLC细胞系和NSCLC患者的原代细胞,探讨miR-143在NSCLC中的作用。将EGFR和miR-143共转染NSCLC细胞,分析EGFR的mRNA和蛋白表达。此外,评估转染癌细胞在集落形成、迁移、侵袭和凋亡方面的活性。与对照组相比,NSCLC细胞系和NSCLC患者原代细胞中miR-143水平降低。用miR-143转染后,NSCLC细胞的增殖、集落形成、迁移和侵袭能力受到抑制。同样,敲低EGFR导致NSCLC细胞增殖受到抑制。miR-143过表达后,EGFR的mRNA和蛋白表达水平显著降低,NSCLC细胞中miR-143水平与EGFR水平呈负相关。本研究结果表明,miR-143能够通过抑制EGFR的作用来抑制NSCLC细胞的增殖和侵袭,提示EGFR可能被视为NSCLC治疗的潜在靶点。