论文已发表
注册即可获取德孚的最新动态
IF 收录期刊
Circ-PRKDC 通过 miR-198/DDR1 调控轴促进结直肠癌的进展
Authors Wang G, Li Y, Zhu H, Huo G, Bai J, Gao Z
Received 30 July 2020
Accepted for publication 28 October 2020
Published 15 December 2020 Volume 2020:12 Pages 12853—12865
DOI https://doi.org/10.2147/CMAR.S273484
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 5
Editor who approved publication: Dr Sanjeev Srivastava
Background: Circular RNAs (circRNAs) play a crucial role in a variety of cancers, including colorectal cancer (CRC). This study aimed to explore the role of hsa_circ_0136666 (circ-PRKDC ) in CRC and its potential mechanism.
Methods: The levels of circ-PRKDC , miR-198 and discoidin domain receptor 1 (DDR1 ) were measured using quantitative real-time polymerase chain reaction or Western blot. Cell viability was detected using cell counting kit-8 (CCK-8) assay. Cell apoptosis and cycle were evaluated via flow cytometry. Cell migration and invasion were examined using transwell assay. CyclinD1 protein level was determined via Western blot. The interaction among circ-PRKDC , miR-198 and DDR1 was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation assay. Xenograft assay was performed to analyze tumor growth in vivo.
Results: Circ-PRKDC and DDR1 levels were increased, and miR-198 level was decreased in CRC tissues and cells. Circ-PRKDC depletion inhibited proliferation, migration and invasion, and expedited apoptosis and cell cycle arrest in SW480 and HCT116 cells. Silence of circ-PRKDC impeded CRC progression by sponging miR-198 . Overexpression of miR-198 hindered CRC development via targeting DDR1 . Moreover, circ-PRKDC silencing suppressed tumor growth in vivo.
Conclusion: Knockdown of circ-PRKDC inhibited CRC progression via modulating miR-198 /DDR1 pathway.
Keywords: colorectal cancer, circ-PRKDC , miR-198 , DDR1 , cell cycle