1Department of Gastroenterology, Huaihe Hospital, Henan University, Kaifeng, 475000 Henan China.
Department of General Surgery, Kaifeng Central Hospital, Kaifeng, Henan China.
Cell Mol Biol Lett. 2019 Jul 27;24:50. doi: 10.1186/s11658-019-0175-8. eCollection 2019.
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.
长链非编码 RNA Malat1 已被广泛鉴定为一种癌基因，其在结直肠癌（CRC）中与肿瘤发生具有显著关系。然而，Malat1 是否参与结直肠癌的自噬仍不清楚。
首先，通过 qRT-PCR 检测 96 对结直肠癌组织和 4 种细胞系中 Malat1 的表达水平。然后，通过 Western blot 检测结直肠癌组织和细胞系中的自噬活性。进一步，通过 CCK-8 assay 和流式细胞术（FCM）检测 Malat1 激活的自噬在结直肠癌细胞系中的作用。
在这项研究中，与相邻正常组织相比，结直肠癌组织中 Malat1 的表达和自噬活性显著增加。此外，Malat1 水平与体内 LC3-II mRNA 的表达呈正相关。而且，Malat1 在结直肠癌细胞中明显促进了自噬激活和细胞增殖，而凋亡减少。最重要的是，3-MA 抑制自噬不仅缓解了 Malat1 诱导的细胞增殖，而且促进了 Malat1 诱导的细胞凋亡。此外，Malat1 被发现作为内源性海绵体，通过直接结合 miR-101 减少 miR-101。此外，Malat1 消除了 miR-101 对 CRC 自噬、增殖和凋亡的抑制作用。
长链非编码 RNA Malat1 通过海绵吸附 miR-101 激活自噬，促进结直肠癌细胞增殖，抑制凋亡。
