Long non-coding RNA Malat1 activated autophagy, hence promoting cell proliferation and inhibiting apoptosis by sponging miR-101 in colorectal cancer

• Published in: Cellular & molecular biology letters Vol. 24; no. 1; p. 50
• Main Authors: Si, Yaoran, Yang, Zhaoguo, Ge, Quanxing, Yu, Lingbing, Yao, Meiying, Sun, Xinfang, Ren, Zheng, Ding, Chunsheng
• Format: Journal Article
• Language: English
• Published: England BioMed Central 27.07.2019; BMC
• Subjects: Apoptosis; Autophagy; Cancer; Cell activation; Cell growth; Cell Line, Tumor; Cell Proliferation; Cholecystokinin; Colorectal cancer; Colorectal carcinoma; Colorectal Neoplasms - genetics; Colorectal Neoplasms - pathology; Flow cytometry; Gene expression; Gene Expression Regulation, Neoplastic; Humans; Long noncoding RNA Malat1; Metastasis; MicroRNAs; MicroRNAs - genetics; miR-101; mRNA; Non-coding RNA; Proliferation; Reagents; RNA, Long Noncoding - genetics; Tumor cell lines; Tumorigenesis; United States > US; Japan; Long noncoding RNA Malat1; Proliferation; Autophagy; Colorectal cancer; miR-101; Apoptosis
• ISSN: 1425-8153; 1689-1392
• DOI: 10.1186/s11658-019-0175-8

Long non-coding RNA Malat1 has been widely identified as an oncogene which shows a significant relationship with tumorigenesis in colorectal cancer (CRC). Nonetheless, whether Malat1 participates in the autophagy of colorectal cancer remains unclear. First, the expression level of Malat1 in 96 pairs of colorectal cancer tissues and four cell lines was detected by qRT-PCR. Subsequently, the autophagy activity in colorectal cancer tissues and cell lines was detected by western blot. Furthermore, the CCK-8 assay and flow cytometry (FCM) were performed to detect the role of autophagy activated by Malat1 in colorectal cancer cell lines. In this study, significantly increased Malat1 expression and autophagy activity were found in colorectal cancer tissues compared with the adjacent normal tissues. Also, the Malat1 level was positively correlated with the expression of LC3-II mRNA in vivo. Moreover, autophagy activation and cell proliferation were significantly facilitated by Malat1 in colorectal cancer cells, while apoptosis decreased. Above all, the inhibition of autophagy by 3-MA not only relieved the Malat1-induced cell proliferation but also promoted the Malat1-induced cell apoptosis. In addition, Malat1 was found to act as an endogenous sponge by directly binding to miR-101 to reduce miR-101. Furthermore, the suppressive effects of miR-101 on the autophagy, proliferation, and apoptosis of CRC were abolished by Malat1. Long non-coding RNA Malat1 activated autophagy and promoted cell proliferation, yet inhibited apoptosis by sponging miR-101 in colorectal cancer cells.