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Research Paper|Volume 11, Issue 5|pp 1389—1403

SP1-induced lncRNA TINCR overexpression contributes to colorectal cancer progression by sponging miR-7-5p

Shaojun Yu1, Da Wang1, Yingkuan Shao2, Teng Zhang3, Haiting Xie1, Xiaomeng Jiang4, Qun Deng1, Yurong Jiao1, Jinhua Yang5, Cheng Cai6, Lifeng Sun1
  • 1Surgical Oncology Department, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, China
  • 2Cancer Institute, Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education, Key Laboratory of Molecular Biology in Medical Sciences, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, China
  • 3Shanghai Tenth People's Hospital, and Department of Pharmacology, Tongji University School of Medicine, Shanghai 200092, China
  • 4Digestive Department, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, Jiangsu Province, China
  • 5Department of Gastrointestinal Tumor Surgery, The Second Affiliated Hospital, Zhejiang University School of Medicine, Changxing Campus, People’s Hospital of Changxing County, Changxing, Zhejiang 313100, China
  • 6Colorectal and Anal Surgery Department, Jinhua Hospital, Zhejiang Uiniversity School of Medicine, Jinhua, Zhejiang 321000, China
Received: November 30, 2018Accepted: February 17, 2019Published: March 10, 2019
https://doi.org/10.18632/aging.101839

Copyright: © 2019 Yu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Mounting evidences have indicated that long noncoding RNAs (lncRNAs) play pivotal roles in human diseases, especially in cancers. Recently, TINCR was proposed to be involved in tumor progression. However, its role in colorectal cancer (CRC) remains elusive. In our study, we found that SP1-induced TINCR was significantly upregulated in CRC tissues and cell lines. Moreover, cox multivariate survival analysis revealed that high TINCR was an independent predictor of poor overall survival (OS). Functionally, knockdown of TINCR obviously suppressed CRC cells proliferation, migration and invasion in vitro, and inhibited CRC cells growth and metastasis in vivo. Mechanistically, we identified TINCR could act as a miR-7-5p sponge using RNA pull down, luciferase reporter and RIP assays. Furthermore, we showed that TINCR might promote CRC progression via miR-7-5p-mediated PI3K/Akt/mTOR signaling pathway. Lastly, we revealed that plasma TINCR expression was upregulated in CRC when compared to healthy controls and could be a promising diagnostic biomarker for CRC. Based on above results, our data indicated that TINCR might serve as a potential diagnostic and prognostic biomarker for CRC.