Carcinogenesis, Teratogenesis & Mutagenesis ›› 2021, Vol. 33 ›› Issue (3): 187-192.doi: 10.3969/j.issn.1004-616x.2021.03.005

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miR-223-3p negatively regulated ECT2 to induce apoptosis in non-small cell lung cancer cells

WANG Xikai1, MENG Qinghe2, GAO Yanlu3   

  1. 1. School of Basic Medical Science, Capital Medical University, Beijing 100069;
    2. School of Public Health, Peking University, Beijing 100191;
    3. The Second Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250001, Shandong, China
  • Received:2021-01-21 Revised:2021-04-27 Online:2021-05-30 Published:2021-06-09

Abstract: OBJECTIVE: To investigate effects of miR- 223- 3p on proliferation and apoptosis of nonsmall cell lung cancer cells. METHODS: Relative expression levels of miR-223-3p were detected by realtime quantitative PCR in 24 patients with non-small cell lung cancer (NSCLC) and expression levels of epithelial transformation sequence 2 (ECT2) protein were analyzed by immunohistochemistry. Correlations between the expression levels of miR-223-3p and ECT2 were analyzed. Human NSCLC cells A549 were divided into normal control group, transfected control group and miR-223-3p over-expression group. The normal control group cells were not treated and cultured normally,and the transfected control group cells were transfected with empty plasmid vector using transfection reagents. The miR-223-3p over-expression group was transfected with miR-223-3p mimics. Proliferation rates of cells from each group were detected by the MTT and the plate colony formation assays. Apoptosis rates of cells in each group were detected by flow cytometry. Expression levels of the ECT2 protein were detected by Western blot assay. After ECT2 was knocked down by siRNA, A549 cells were divided into normal control, transfected control and ECT2 silenced groups. Then, changes of cell proliferation and apoptosis in each group were detected. RESULTS: Expressions of miR-223- 3p in cancer tissues were significantly lower than that in paracancerous tissues while expressions of ECT2 protein were higher, showing a negative correlation between them (r=- 0.666, P < 0.05). Compared with the normal control and the transfected control groups, proliferation rates of miR- 223- 3p in the over- expression group was decreased (P < 0.05),expressions of ECT2 protein were significantly decreased,and apoptosis rates were significantly increased (P < 0.05). Effects from siRNA knockdown of ECT2 on cell proliferation and apoptosis were basically the same as that of miR- 223-3p over-expression group. CONCLUSION: Our data show that miR- 223-3p inhibited proliferation and induced apoptosis of NSCLC cells by negatively regulating the expression of ECT2.

Key words: miR-223-3p, ECT2, non-small cell lung cancer, apoptosis

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