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
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
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