Tianjin Med J ›› 2016, Vol. 44 ›› Issue (8): 984-987.doi: 10.11958/20150421

• Cell and Molecular Biology • Previous Articles     Next Articles

miR-200b suppresses proliferation and induces apoptosis in non-small cell lung cancer cells by targeting DNMT3A

LUO Weimin, LUO Xiangyu, GUO Jialong, LIN Chengyi, ZHANG Jun△   

  1. Department of Cardiothoracic Surgery, the Affiliated Shiyan Taihe Hospital of Hubei College of Pharmacy, Shiyan 442000, China
  • Received:2016-01-05 Revised:2016-03-01 Published:2016-08-15 Online:2016-08-22
  • Contact: ZHANG Jun E-mail: dengmin2006@163.com E-mail:2319218424@qq.com

Abstract: Abstract: Objective To investigate whether miR-200b suppresses proliferation and induces apoptosis of non-small cell lung cancer cells by targeting DNMT3A. Methods A qRT-PCR was employed for detecting the expression of miR-200b in different non-small cell lung cancer cells and human bronchial epithelial cells. A549 cells were transfected with miR-200b mimics, scramble, DNMT3A-siRNA and control-siRNA, respectively. The scramble and control-siRNA were served the negative control of miR-200b mimics and DNMT3A-siRNA, respectively. Western blot assay was conducted to detect the expression of DNMT3A protein in A549 cells. MTT and Annexin V/propidium iodide staining were employed to detect the proliferation ability and apoptosis rate of A549 cells. The effects of miR-200b mimics and DNMT3A-siRNA on the proliferation and apoptosis rate of A549 cells were compared between groups. Results Results of qRT-PCR showed that the expression of miR-200b was significantly down-regulated in A549, H1299, L78 and H460 cells than that of 16HBE cells. Among them, the most obviously reduction was found in A549 cells (P < 0.05). Western blot assay showed that the level of DNMT3A protein was inhibited by restored miR-200b or knock-down DNMT3A in A549 cells. After transfection of miR-200bmimics or knock-downDNMT3Afor 48 h, 72 h and 96 h,MTT showed that theODvalues, which reflected the optical density of cell proliferationwere significantly lower than those in the control group (P < 0.05). Annexin V/propidiumiodide staining showed that apoptosis rates of A549 cells after transfection of miR-200bmimics or knock-downDNMT3Awere (23.33%±0.90%and 20.41%±0.70%), comparedwith the control group (5.28%± 0.55%and 5.68%±0.47%, P < 0.01). Conclusion miR-200b suppresses cell proliferation and induces apoptosis by targeting DNMT3Ain non-small cell lung cancer.

Key words: microRNAs, carcinoma, non-small-cell lung, cell proliferation, apoptosis, miR-200b, DNMT3A