Yin J, Ye YL, Hu T, Xu LJ, Zhang LP, Ji RN, Li P, Chen Q, Zhu JY, Pang Z. Hsa_circRNA_102610 upregulation in Crohn’s disease promotes transforming growth factor-β1-induced epithelial-mesenchymal transition via sponging of hsa-miR-130a-3p. World J Gastroenterol 2020; 26(22): 3034-3055 [PMID: 32587447 DOI: 10.3748/wjg.v26.i22.3034]
Corresponding Author of This Article
Zhi Pang, PhD, Chief Doctor, Full Professor, Department of Gastroenterology, The North District of the Affiliated Suzhou Hospital of Nanjing Medical University, 242 Guangji Road, Suzhou 215008, Jiangsu Province, China. pangzhi0273@sina.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
Share the Article
Yin J, Ye YL, Hu T, Xu LJ, Zhang LP, Ji RN, Li P, Chen Q, Zhu JY, Pang Z. Hsa_circRNA_102610 upregulation in Crohn’s disease promotes transforming growth factor-β1-induced epithelial-mesenchymal transition via sponging of hsa-miR-130a-3p. World J Gastroenterol 2020; 26(22): 3034-3055 [PMID: 32587447 DOI: 10.3748/wjg.v26.i22.3034]
World J Gastroenterol. Jun 14, 2020; 26(22): 3034-3055 Published online Jun 14, 2020. doi: 10.3748/wjg.v26.i22.3034
Hsa_circRNA_102610 upregulation in Crohn’s disease promotes transforming growth factor-β1-induced epithelial-mesenchymal transition via sponging of hsa-miR-130a-3p
Juan Yin, Yu-Lan Ye, Tong Hu, Li-Juan Xu, Li-Ping Zhang, Ru-Ning Ji, Ping Li, Qian Chen, Jian-Yun Zhu, Zhi Pang
Juan Yin, Ping Li, Qian Chen, Jian-Yun Zhu, Zhi Pang, Department of Digestive Disease and Nutrition Research Center, the Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou 215008, Jiangsu Province, China
Yu-Lan Ye, Tong Hu, Li-Juan Xu, Li-Ping Zhang, Zhi Pang, Department of Gastroenterology, the Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou 215008, Jiangsu Province, China
Ru-Ning Ji, Department of Biomedical Engineering, the Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou 215008, Jiangsu Province, China
Author contributions: Pang Z and Yin J designed this study; Zhu JY guided experimental methods; Ye YL, Hu T, Xu L and Zhang LP collected the samples; Yin J carried out the experiments; Li P, Qian C and Ji RN helped with data analysis; Yin J wrote the manuscript; Pang Z, Ye YL and Zhu JY revised the manuscript; all authors approved the final version of the article.
Supported bythe Suzhou Special Project of Diagnosis and Treatment for Key Clinical Disease, No. LCZX201715; the Natural Science Foundation of Jiangsu Province, No. BK20161232; and the Science and Technology Development Fund of Nanjing Medical University, No. NMUB2018215.
Institutional review board statement: The study was reviewed and approved by the Institutional Review Board at the Ethics Committee of the Affiliated Suzhou Hospital of Nanjing Medical University.
Institutional animal care and use committee statement: No animal experiments were conducted in this study.
Conflict-of-interest statement: The authors declare there are no conflicts of interest.
Data sharing statement: No additional data are available.
Corresponding author: Zhi Pang, PhD, Chief Doctor, Full Professor, Department of Gastroenterology, The North District of the Affiliated Suzhou Hospital of Nanjing Medical University, 242 Guangji Road, Suzhou 215008, Jiangsu Province, China. pangzhi0273@sina.com
Received: February 11, 2020 Peer-review started: February 11, 2020 First decision: March 26, 2020 Revised: April 10, 2020 Accepted: April 24, 2020 Article in press: April 24, 2020 Published online: June 14, 2020 Processing time: 124 Days and 10.6 Hours
Core Tip
Core tip: The incidence of inflammatory bowel disease, a chronic intestinal inflammatory disorder that includes Crohn’s disease (CD) and ulcerative colitis is rising. Our previous study revealed that hsa_circRNA_102610 is upregulated in CD patients. However, further investigation is required to explore how hsa_circRNA_102610 participates in the pathogenesis of CD. The results of this study indicate that hsa_circRNA_102610 overexpression in CD patients could accelerate the proliferation and epithelial-mesenchymal transition of intestinal epithelial cells via sponging of hsa-miR-130a-3p. Thus, hsa_circRNA_102610 may promote CD progression. Hsa_circRNA_102610 may serve as a potential target for CD therapy and novel drug research. Exogenously delivered hsa-miR-130a-3p could possibly act as a sponge of hsa_circRNA_102610.