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DICER1-AS1 Promotes the Malignant Behaviors of Colorectal Cancer Cells by Regulating miR-296-5p/STAT3 Axis

Authors Ma C, Ma N, Qin L, Miao C, Luo M, Liu S

Received 6 March 2020

Accepted for publication 10 July 2020

Published 13 October 2020 Volume 2020:12 Pages 10035—10046

DOI https://doi.org/10.2147/CMAR.S252786

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 4

Editor who approved publication: Dr Sanjeev Srivastava


Chuanyu Ma,1 Ning Ma,1 Lili Qin,1 Chuanna Miao,1 Minglei Luo,1 Shuhong Liu2

1Department of Proctology, Linyi Central Hospital, Linyi, Shandong Province, People’s Republic of China; 2Department of Radiotherapy, Linyi Cancer Hospital, Linyi, Shandong Province, People’s Republic of China

Correspondence: Shuhong Liu
Department of Radiotherapy, Linyi Cancer Hospital, Lingyuan East Street No. 6, Lanshan District, Linyi 276400, Shandong Province, People’s Republic of China
Email yiyan0663363@163.com

Background: Long non-coding RNA (lncRNA) exerts a regulatory role in the occurrence and progression of tumors. This study aimed at probing into the function and mechanism of lncRNA DICER1 antisense RNA 1 (DICER1-AS1) in colorectal cancer (CRC).
Methods: The expressions of DICER1-AS1, miR-296-5p and STAT3 mRNA were tested by quantitative real-time polymerase chain reaction (qRT-PCR). Cell counting kit-8 (CCK-8) assay was employed to detect cell proliferation, and Transwell was used to detect cell migration and invasion. In addition, the expressions of apoptosis-related proteins Bax and Bcl2 were detected by Western blot. Interactions between DICER1-AS1 and miR-296-5p, and miR-296-5p and STAT3 were predicted and determined by bioinformatics analysis, luciferase reporter assay and RNA binding protein immunoprecipitation (RIP) assay.
Results: The expressions of DICER1-AS1 and STAT3 mRNA were significantly up-regulated while miR-296-5p expression was remarkably down-regulated in CRC tissues and cell lines. Over-expression of DICER1-AS1 or transfection of miR-296-5p inhibitors could promote the proliferation, migration and invasion and inhibit apoptosis of CRC cells, whereas knockdown of DICER1-AS1 or transfection of miR-296-5p mimics had the opposite effects. Additionally, DICER1-AS1 could down-regulate miR-296-5p expression via sponging it. DICER1-AS1 also enhanced the expression of STAT3, which was identified as a target gene of miR-296-5p.
Conclusion: DICER1-AS1 acts as an oncogenic lncRNA in CRC via modulating miR-296-5p/STAT3 axis. Our results provide a new direction for the diagnosis and treatment of CRC.

Keywords: DICER1-AS1, miR-296-5p, CRC, proliferation, metastasis

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