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]
日期:2019-03-01
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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