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

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 potenti...

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Published in:PloS one Vol. 11; no. 7; p. e0158347
Main Authors: Yu, Lei, Gong, Xuejun, Sun, Lei, Zhou, Qiying, Lu, Baoling, Zhu, Liying
Format: Journal Article
Language:English
Published: United States Public Library of Science 08.07.2016
Public Library of Science (PLoS)
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ISSN:1932-6203, 1932-6203
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Summary: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.
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Conceived and designed the experiments: LY XG LS QZ BL LZ. Performed the experiments: LY XG LS QZ BL LZ. Analyzed the data: LY XG LS QZ BL LZ. Contributed reagents/materials/analysis tools: LY XG LS QZ BL LZ. Wrote the paper: LY XG LS QZ BL LZ.
Competing Interests: The authors have declared that no competing interests exist.
These authors are joint first authors on this work.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0158347