Abstract
BackgroundLong 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.Materials and methodsFirst, 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.ResultsIn 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.ConclusionLong non-coding RNA Malat1 activated autophagy and promoted cell proliferation, yet inhibited apoptosis by sponging miR-101 in colorectal cancer cells.
Highlights
Long non-coding RNA (LncRNAs) and non-coding RNAs longer than 200 nucleotides [1, 2] function by interacting and regulating various types of genes and proteins via diverse mechanisms [3], thereby participating in a variety of fundamental physiopathologic processes, such as carcinogenesis, autophagy, cardiovascular and neurological diseases [4,5,6]
The suppressive effects of miR-101 on the autophagy, proliferation, and apoptosis of colorectal cancer (CRC) were abolished by Metastasis-associated lung adenocarcinoma transcript 1 (Malat1)
Malat1 was remarkably overexpressed in CRC, and associated with autophagy activation in CRC Ninety-six pairs of CRC tissues and adjacent normal tissues were detected by quantitative real-time PCR (qRT-PCR) to reveal the role of Malat1 in CRC
Summary
Long non-coding RNA (LncRNAs) and non-coding RNAs longer than 200 nucleotides [1, 2] function by interacting and regulating various types of genes and proteins via diverse mechanisms [3], thereby participating in a variety of fundamental physiopathologic processes, such as carcinogenesis, autophagy, cardiovascular and neurological diseases [4,5,6]. Numerous studies have demonstrated that as a self-protective mechanism, autophagy can be regulated by lncRNA in cancer cells. Increasing reports have indicated that Malat activates autophagy and participates in tumorigenesis, such as cell proliferation, apoptosis and metastasis, in a number of cancer cells [9, 14,15,16,17,18]. Whether Malat participates in the autophagy of colorectal cancer remains unclear
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