MicroRNA-34a inhibits the proliferation and promotes the apoptosis of non-small cell lung cancer H1299 cell line by targeting TGF[beta]R2

• Published in: Tumor biology Vol. 36; no. 4; p. 2481
• Main Authors: Ma, Zhong-liang, Hou, Pin-pin, Li, Yan-li, Wang, De-tao, Yuan, Tian-wei, Wei, Jia-li, Zhao, Bo-tao, Lou, Jia-tao, Zhao, Xin-tai, Jin, Yan, Jin, You-xin
• Format: Journal Article
• Language: English
• Published: London Springer Nature B.V 01.04.2015
• Subjects: Apoptosis; Gene expression; Lung cancer; MicroRNAs
• ISSN: 1010-4283; 1423-0380
• DOI: 10.1007/s13277-014-2861-5

MicroRNAs (MiRNAs) are small non-coding RNA molecules which act as important regulators of post-transcriptional gene expression by binding 3'-untranslated region (3'-UTR) of target messenger RNA (mRNA). In this study, we analyzed miRNA-34a (miR-34a) as a tumor suppressor in non-small cell lung cancer (NSCLC) H1299 cell line. The expression level of miR-34a in four different NSCLC cell lines, H1299, A549, SPCA-1, and HCC827, was significantly lower than that in the non-tumorigenic bronchial epithelium cell line BEAS-2B. In human NSCLC tissues, miR-34a expression level was also significantly decreased in pT2-4 compared with the pT1 group. Moreover, miR-34a mimic could inhibit the proliferation and triggered apoptosis in H1299 cells. Luciferase assays revealed that miR-34a inhibited TGF[beta]R2 expression by targeting one binding site in the 3'-UTR of TGF[beta]R2 mRNA. Quantitative real-time PCR (qRT-PCR) and Western blot assays verified that miR-34a reduced TGF[beta]R2 expression at both mRNA and protein levels. Furthermore, downregulation of TGF[beta]R2 by siRNA showed the same effects on the proliferation and apoptosis as miR-34a mimic in H1299 cells. Our results demonstrated that miR-34a could inhibit the proliferation and promote the apoptosis of H1299 cells partially through the downregulation of its target gene TGF[beta]R2.