• Hua Wei, Zhichao Yang, and Bo Lin.
• Department of Endoscopy, Huaihe Hospital, Henan University, Kaifeng, China.
• Gene. 2019 Mar 1; 687: 9-15.

AimsIn previous studies, dysregulated lncRNAs in colorectal cancer were screened using RNA-sequencing by Atsushi Yamada. In these dysregulated lncRNAs, a long non coding RNA named CA3-AS1 attracted our attention due to its high conservation and fold change, which was downregulated in colorectal cancer. In this study, we aimed to investigate the function and mechanism of lncRNA CA3-AS1 in colorectal cancer.MethodsRT-PCR was used to detect CA3-AS1, miR-93, PTEN mRNA expression. Apoptosis, proliferation, and invasion were examined by western blotting, CCK8, transwell assay to evaluate the function of RPL34-AS1.ResultsWe found that lncRNA CA3-AS1 mainly located in cytoplasm, and overexpression of lncRNA CA3-AS1 inhibits cell proliferation, invasion and promotes cell apoptosis. Our results revealed that miR-93 could directly bind to CA3-AS1, and verified the oncogenic role of miR-93. Furthermore, we found that miR-93 played its role through regulating PTEN, the tumor-suppressor gene, which was inversely correlated with miR-93.ConclusionBased on the investigation, lncRNA CA3-AS1 inhibited the proliferation, invasion and apoptosis, which could be blocked by overexpression of miR-93. In summary, our study demonstrated that CA3-AS1/miR-93/PTEN axis may play an important role in the regulation of colorectal cancer progression, which provides new insights for clinical treatment.Copyright © 2018. Published by Elsevier B.V.

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