Wu MN, Zheng WJ, Ye WX, Wang L, Chen Y, Yang J, Yao DF, Yao M. Oncogenic tuftelin 1 as a potential molecular-targeted for inhibiting hepatocellular carcinoma growth. World J Gastroenterol 2021; 27(23): 3327-3341 [PMID: 34163115 DOI: 10.3748/wjg.v27.i23.3327]
Corresponding Author of This Article
Deng-Fu Yao, MD, PhD, Director, Full Professor, Research Center of Clinical Medicine, The Affiliated Hospital of Nantong University, No. 20 West Temple Road, Nantong 226001, Jiangsu Province, China. yaodf@ahnmc.com
Research Domain of This Article
Oncology
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/
World J Gastroenterol. Jun 21, 2021; 27(23): 3327-3341 Published online Jun 21, 2021. doi: 10.3748/wjg.v27.i23.3327
Oncogenic tuftelin 1 as a potential molecular-targeted for inhibiting hepatocellular carcinoma growth
Meng-Na Wu, Wen-Jie Zheng, Wen-Xin Ye, Li Wang, Ying Chen, Jie Yang, Deng-Fu Yao, Min Yao
Meng-Na Wu, Wen-Jie Zheng, Deng-Fu Yao, Research Center of Clinical Medicine, The Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China
Wen-Xin Ye, Min Yao, Department of Medical Immunology, Medical School of Nantong University, Nantong 226001, Jiangsu Province, China
Li Wang, Department of Medical Informatics, Medical School of Nantong University, Nantong 226001, Jiangsu Province, China
Ying Chen, Department of Oncology, The Affiliated Second Hospital of Nantong University, Nantong 226001, Jiangsu Province, China
Jie Yang, Department of Molecular Biology, Life Science School of Nantong University, Nantong 226009, Jiangsu Province, China
Author contributions: Wu MN, Zheng WJ, and Ye WX contributed equally to this work and wrote the first draft; Wang L, Chen Y, and Yang J contributed to the methodology, data curation, and formal analysis; Yao M and Yao DF revised the manuscript. All authors approved the final version of the manuscript.
Supported byProjects of the Ministry of Science and Technology, National Key Research and Development Program, No. 2018YFC0116902; National Natural Science Foundation of China, No. 81673241, No. 31872738, No. 81873915.
Institutional review board statement: This study was approved by the Ethics Committee of the Affiliated Hospital of Nantong University (TDFY2018-025), China.
Conflict-of-interest statement: No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (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/
Corresponding author: Deng-Fu Yao, MD, PhD, Director, Full Professor, Research Center of Clinical Medicine, The Affiliated Hospital of Nantong University, No. 20 West Temple Road, Nantong 226001, Jiangsu Province, China. yaodf@ahnmc.com
Received: December 14, 2020 Peer-review started: December 14, 2020 First decision: December 27, 2020 Revised: January 6, 2021 Accepted: May 19, 2021 Article in press: May 19, 2021 Published online: June 21, 2021 Processing time: 185 Days and 22.1 Hours
Core Tip
Core Tip: Tuftelin1 (TUFT1) has been reported to be regulated by hypoxia and involved in the Hedgehog signaling pathway, with over-expression in hepatocellular carcinoma (HCC) tissues or cell lines. Abnormal TUFT1 level was significantly related to tumor size, vascular invasion, positive hepatitis B e-antigen, advanced tumor-node-metastasis stage of HCC, patients with ascites, and shorter overall survival and disease-free survival. Interfering TUFT1 transcription could markedly suppress the growth and metastasis of high TUFT1 MHCC-97H cell lines in vitro through accelerating apoptosis. Moreover, increasing TUFT1 expression might promote the growth and metastasis of low TUFT1 Hep3B cell lines in vitro. The data suggested that TUFT1 is involved in HCC progression via the mechanism of inhibiting apoptosis and might serve as a potential therapeutic target for inhibiting HCC growth.