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MiR-193a-3p inhibits pancreatic ductal adenocarcinoma cell proliferation by targeting CCND1

Authors Chen ZM, Yu Q, Chen G, Tang RX, Luo DZ, Dang YW, Wei DM

Received 22 December 2018

Accepted for publication 29 March 2019

Published 27 May 2019 Volume 2019:11 Pages 4825—4837


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Antonella D'Anneo

Zhi-Min Chen,* Qiao Yu,* Gang Chen, Rui-Xue Tang, Dian-Zhong Luo, Yi-Wu Dang, Dan-Ming Wei

Department of Pathology, First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China

*These authors contributed equally to this work

MicroRNAs (miRNAs) could modulate gene expression at the posttranscriptional level by promoting mRNA degradation or blocking mRNA translation, thus affecting the occurrence and development of cancer.
Methods: In this work, qRT-PCR was conducted to detect the expression of miR-193a-3p and CCND1. The ability of cell proliferation was evaluated via CCK-8 assay. Cell apoptosis and cell cycle distribution were detected by flow cytometry. Bioinformatic techniques were employed to research the regulatory relationship between miR-193a-3p and target genes. The relationship between miR-193a-3p and CCND1 was verified via dual-luciferase reporter assays.
Results: MiR-193a-3p expression in pancreatic ductal adenocarcinoma (PDAC) tissue was significantly lower than in non-cancerous tissue. After overexpressing miR-193a-3p in PDAC cells, their multiplication ability was significantly inhibited, apoptosis was accelerated, and the cell cycle was blocked in the G1 and G2/M phases. CCND1 was confirmed to have a targeted relationship with miR-193a-3p. Moreover, CCND1 expression was significantly lower in PDAC cells with an overexpression of miR-193a-3p.
Conclusions: MiR-193a-3p targeted CCND1 to suppress tumor growth in PDAC cells. MiR-193a-3p may function as a tumor inhibitor in PDAC development, which could offer a promising therapeutic and prognostic strategy for PDAC treatment.

Keywords: miR-193a-3p, CCND1, PDAC, proliferation

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