The Circular RNA Cdr1as Act as an Oncogene in Hepatocellular Carcinoma through Targeting miR-7 Expression

Lei Yu; Xuejun Gong; Lei Sun; Qiying Zhou; Baoling Lu; Liying Zhu

doi:10.1371/journal.pone.0158347

The Circular RNA Cdr1as Act as an Oncogene in Hepatocellular Carcinoma through Targeting miR-7 Expression

PLoS One. 2016 Jul 8;11(7):e0158347. doi: 10.1371/journal.pone.0158347. eCollection 2016.

Authors

Lei Yu¹, Xuejun Gong², Lei Sun³, Qiying Zhou⁴, Baoling Lu¹, Liying Zhu¹

Affiliations

¹ Department of Infectious Disease,The Fourth Hospital of Harbin Medical University, Harbin 150001, Heilongjiang, China.
² Department of Biliary and Pancreatic Surgery, Xiangya Hospital of Central South University, Changsha, 410008, Hunan, China.
³ Department of Ophthalmology,The Fourth Hospital of Harbin Medical University, Harbin 150001, Heilongjiang, China.
⁴ College of Computer Science and Technology (Network and Information Security), JiLin University, Changchun, 130001, Jilin, China.

Abstract

CircRNAs are a class of endogenous RNA that regulates gene expression at the post-transcriptional or transcriptionallevel through interacting with other molecules or microRNAs. Increasing studies have demonstrated that circRNAs play a crucial role in biology processes. CircRNAs are proved as potentialbiomarkers in many diseases including cancers. However, the role of Cdr1as in Hepatocellular carcinoma (HCC) remains to be elucidated. We demonstrated that Cdr1as expression was upregulated in HCC tissues compared with the adjacent non-tumor tissues. In addtion, miR-7 expression was downregulated in HCC tissues compared with the adjacent non-tumor tissues. Moreover, the expression level of miR-7 was inversely correlated with that in HCC tissues. Knockdown of Cdr1as suppressed the HCC cell proliferation and invasion. Overexpression of miR-7 inhibited the HCC cell proliferation and invasion. Overexpression of miR-7 could suppress the direct target gene CCNE1 and PIK3CD expression. Knockdown of Cdr1as suppressed the expression of miR-7 and also inhibited the CCNE1 and PIK3CD expression. Furthermore, knockdown of Cdr1as suppressed the HCC cell proliferation and invasion through targeting miR-7. These data suggested that Cdr1as acted as an oncogene partly through targeting miR-7 in HCC.

Publication types

Retracted Publication

MeSH terms

Carcinoma, Hepatocellular / genetics
Carcinoma, Hepatocellular / metabolism*
Carcinoma, Hepatocellular / pathology
Cell Proliferation / genetics
Class I Phosphatidylinositol 3-Kinases / biosynthesis
Class I Phosphatidylinositol 3-Kinases / genetics
Female
Gene Expression Regulation, Neoplastic*
Humans
Liver Neoplasms / genetics
Liver Neoplasms / metabolism*
Liver Neoplasms / pathology
Male
MicroRNAs / biosynthesis*
MicroRNAs / genetics
Neoplasm Invasiveness
Neoplasm Proteins / biosynthesis
Neoplasm Proteins / genetics
Oncogenes*
RNA, Long Noncoding / genetics
RNA, Long Noncoding / metabolism*
RNA, Neoplasm / genetics
RNA, Neoplasm / metabolism*
Tumor Cells, Cultured

Substances

MIRN7 microRNA, human
MicroRNAs
Neoplasm Proteins
RNA, Long Noncoding
RNA, Neoplasm
long non-coding RNA CDR1AS, human
Class I Phosphatidylinositol 3-Kinases
PIK3CD protein, human

Grants and funding

This work was supported by the Postdoctoral scientific research developmental fund of Heilongjiang Province (No. LBH-Q14115), and sponsored by National Science and Technology Major Project (2014ZX10002002) and Natural Science Foundation of Heilongjiang Province (ZD2015019), URL: http://jj.hljkj.cn/zr/. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.