Downregulation of miR-216a-5p by long noncoding RNA PVT1 suppresses colorectal cancer progression via modulation of YBX1 expression
Authors Zeng X, Liu Y, Zhu H, Chen D, Hu W
Received 16 March 2019
Accepted for publication 7 June 2019
Published 24 July 2019 Volume 2019:11 Pages 6981—6993
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Cristina Weinberg
Peer reviewer comments 2
Editor who approved publication: Dr Kenan Onel
Xiang Zeng,1,* Yan Liu,2,* Hongquan Zhu,1 Di Chen,1 Weimin Hu1
1Gastrointesitinal Oncosurgery, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou, People’s Republic of China; 2Clinical Laboratory, Guangdong Women’s and Children’s Hospital, Guangzhou, People’s Republic of China
*These authors contributed equally to this work
Purpose: Increasing evidence has demonstrated that microRNAs (miRNAs) are closely related to the occurrence and development of tumors. MiR-216a-5p, located at 2p16.1, has been shown to suppress proliferation of cancerous cells. However, its expression and function in colorectal cancer (CRC) remain unclear.
Materials and methods: The significance of miR-216a-5p in CRC was studied by analyzing miR-216a-5p expression in CRC tissues and its association with clinicopathological parameters. CRC cells, stably overexpressing miR-216a-5p, were evaluated for cell proliferation and metastasis using cell counting kit-8 (CCK-8) and transwell assay methods. Epithelial–mesenchymal transition (EMT) pathway was analyzed by Western blotting. Bioinformatics, quantitative real-time polymerase chain reaction (RT-qPCR), and luciferase reporter assay were performed to define the regulation of PVT1/miR-216a-5p/Y Box Binding Protein 1 (YBX1) axis in CRC.
Results: The expression of miR-216a-5p was found to be significantly downregulated in CRC and was correlated with the various stages and differentiation degree of the tumors. Moreover, the overexpression of miR-216a-5p could significantly inhibit the tumor growth, metastasis, and EMT progression in CRC. Furthermore, the expression of miR-216a-5p was negatively correlated with the expression of PVT1, and PVT1 could reverse tumor suppressive effect of miR-216a-5p in CRC cells. Finally, YBX1 might be the key target of PVT1/miR-216a-5p axis in CRC.
Conclusion: Downregulation of miR-216a-5p by PVT1 could suppress CRC progression via modulating YBX1 expression.
Keywords: colorectal cancer, PVT1, miR-216a-5p, YBX1, epithelial–mesenchymal transition, metastasis
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