Back to Journals » OncoTargets and Therapy » Volume 13

The Long Non-Coding RNA-RoR Promotes the Tumorigenesis of Human Colorectal Cancer by Targeting miR-6833-3p Through SMC4

Authors Li X, Chen W, Jia J, You Z, Hu C, Zhuang Y, Lin Z, Liu Y, Yang C, Xu R

Received 17 November 2019

Accepted for publication 3 February 2020

Published 27 March 2020 Volume 2020:13 Pages 2573—2581


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Sanjeev Srivastava

Xinyu Li,1,* Wen Chen,2,* Jing Jia,1,* Zhicheng You,3 Changjin Hu,4 Yihuang Zhuang,1 Zhibin Lin,1 Yan Liu,1 Chunkang Yang,5 Rongyu Xu1

1Quanzhou First Hospital, Quanzhou, Fujian Province, People’s Republic of China; 2The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, People’s Republic of China; 3Yongchun County Hospital, Quanzhou, Fujian Province, People’s Republic of China; 4Jinjiang Hospital of Traditional Chinese Medicine Affiliated to Fujian University of Traditional Chinese Medicine, Jinjiang, Fujian Province, People’s Republic of China; 5Fujian Tumor Hospital, Fuzhou, Fujian Province, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Chunkang Yang
Department of Gastroenterology, Fujian Tumor Hospital, Fuzhou, Fujian Province, People’s Republic of China
Rongyu Xu
Department of Surgical Oncology, Quanzhou First Hospital, Quanzhou, Fujian Province, People’s Republic of China

Background: Long non-coding RNA regulator of reprogramming (LINC-RoR) has shown different expressions in a variety of tumors as a stem cell inducer through reprogramming regulation. However, its role and regulation mechanisms in colorectal cancer (CRC) are still unclear.
Materials and Methods: Quantitative real-time PCR and Western blot were performed to examine LINC-RoR expression in paired CRC samples and cell lines. The relationship of LINC-RoR expression with clinicopathological characteristics and clinical outcomes was analyzed. The biological functions of LINC-RoR were studied by MTS and colony formation in vitro. Cell apoptosis was analysed by the flow cytometry. The Dual-luciferase reporter assays and RIP assays were performed to explore the regulatory relationship of LINC-RoR.
Results: In this study, we found that LINC-RoR was upregulated in CRC cell lines and tissues. High expression of LINC-RoR was associated with poorer survival time and multivariate analysis results showed that LINC-RoR was an independent risk factor of tumor malignancy progression. Overexpression of LINC-RoR promoted the cell proliferation and knocked down it can reverse the effect in vitro. The regulatory network of LINC-ROR/miR-6833-3p/SMC4 was predicted with bioinformatics analysis tools and validated via dual-luciferase reporter assays and RIP. Further study revealed that in overexpression LINC-RoR cell lines the expression of miR-6833-3p was downregulated and miR-6833-3p can inhibit its target gene SMC4, the apoptosis-related protein.
Conclusion: We concluded that LINC-RoR functions as an oncogene in CRC through the miR-6833-3p/SMC4 pathway.

Keywords: LINC-RoR, colorectal cancer, miR-6833-3p, SMC4, non-coding RNA, apoptosis

Creative Commons License This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

Download Article [PDF]  View Full Text [HTML][Machine readable]