Overexpression of long non coding RNA CA3-AS1 suppresses proliferation, invasion and promotes apoptosis via miRNA-93/PTEN axis in colorectal cancer

PTEN公司 生物 长非编码RNA 小RNA 癌症研究 结直肠癌 细胞凋亡 细胞生长 反义RNA 核糖核酸 竞争性内源性RNA 癌症 基因 遗传学 PI3K/AKT/mTOR通路
作者
Wei Hua,Zhi-Chao Yang,Bo Lin
出处
期刊:Gene [Elsevier BV]
卷期号:687: 9-15 被引量:21
标识
DOI:10.1016/j.gene.2018.11.008
摘要

In 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. RT-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. We 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. Based 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.

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