Tianjin Medical Journal ›› 2020, Vol. 48 ›› Issue (12): 1146-1152.doi: 10.11958/20202143

• Cell and Molecular Biology • Previous Articles     Next Articles

LncRNA-MALAT1 regulates the proliferation and apoptosis of colorectal cancer cells through the miR-142-3p/TEAD1 molecular axis

ZHANG Zhi-cheng, YANG Qing-quan   

  1. Department of General Surgery, the Second Affiliated Hospital of Shenyang Medical College, Shenyang 110002, China
  • Received:2020-07-27 Revised:2020-09-06 Published:2020-12-15 Online:2020-12-13
  • Contact: YANG Qing-quan E-mail:yqqsy@163.com

Abstract: Objective To explore the effect and related mechanisms of LncRNA-MALAT1 on the proliferation and apoptosis of colorectal cancer cells. Methods The expressions of LncRNA-MALAT1 gene, miR-142-3p gene and TEAD1 protein in colorectal cancer cell lines and human normal colon epithelial cells were detected by Real-time PCR and Western blot experiments. Si-MALAT1 was transfected into HCT116 cells, and miR-142-3p inhibitor was co-transfected with si-MALAT1 into HCT116 cells on this basis. Real-time PCR and Western blot techniques were used to detect the expressions of LncRNA-MALAT1 gene, miR-142-3p gene, TEAD1 protein, Bax protein, Bcl-2 protein and Cyclin D1 protein in HCT116 cells. The level of cell proliferation was detected by CCK-8 assay, and the level of cell apoptosis in HCT116 cells was detected by flow cytometry. The dual luciferase experiment was used to detect the binding of LncRNA-MALAT1 and miR-142-3p, miR-142-3p and TEAD1 in HCT116 cells. Results Compared with human normal colon epithelial cells, LncRNA-MALAT1 gene and TEAD1 protein were expressed at high levels and miR-142-3p gene was expressed at a low level in colorectal cancer cell lines. Silencing of LncRNA-MALAT1 could promote the expressions of miR-142-3p gene and Bax protein, inhibit the expressions of LncRNA-MALAT1 gene, Bcl-2 protein, Cyclin D1 protein and TEAD1 protein, inhibit the level of cell proliferation and promote the level of cell apoptosis in HCT116 cells. Co-silencing of miR-142-3p and LncRNA-MALAT1 could partially reverse the above regulatory effects. The binding of LncRNA-MALAT1 and miR-142-3p, miR-142-3p and TEAD1 in HCT-116 cells were detected by the dual luciferase experiment. Conclusion LncRNA-MALAT1 could promote the expression of miR-142-3p target gene TEAD1, promote the capacity of proliferation in colorectal cancer cells, inhibit the level of apoptosis in colorectal cancer cells, and then promote the pathological process of colorectal cancer by binding to miR-142-3p.

Key words: colorectal neoplasms, cell proliferation, apoptosis, microRNAs, RNA, long noncoding, metastasis-associated lung adenocarcinoma transcript 1, TEA domain transcription factor 1

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