期刊
GENE
卷 687, 期 -, 页码 9-15出版社
ELSEVIER
DOI: 10.1016/j.gene.2018.11.008
关键词
CA3-AS1; miR-93; PTEN; Colorectal cancer
资金
- Kaifeng Social Development and Science Technology Research Project [1603065]
Aims: In previous studies, dysregulated IncRNAs 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 IncRNA CA3-AS1 in colorectal cancer. Methods: 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. Results: We found that IncRNA 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. Conclusion Based on the investigation, 1ncRNA 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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