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©The Author(s) 2019. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Feb 28, 2019; 25(8): 923-940
Published online Feb 28, 2019. doi: 10.3748/wjg.v25.i8.923
Published online Feb 28, 2019. doi: 10.3748/wjg.v25.i8.923
Dbx2 exhibits a tumor-promoting function in hepatocellular carcinoma cell lines via regulating Shh-Gli1 signaling
Yan-Ting Hu, Bei-Fang Li, Yan-Yan Li, Lin Shen, Jing Gao, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Gastrointestinal Oncology, Peking University Cancer Hospital and Institute, Beijing 100142, China
Peng-Jun Zhang, Di Wu, Xu Zhu, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Interventional Therapy, Peking University Cancer Hospital and Institute, Beijing 100142, China
Bin Dong, Key laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Pathology, Peking University Cancer Hospital and Institute, Beijing 100142, China
Author contributions: Zhu X and Gao J designed and conceived the study; Hu YT and Li BF performed the experiments; Zhang PJ, Wu D, and Dong B analyzed and interpreted the data; Li YY, Li ZW, and Shen L offered the reagents, materials, and analysis tools; Hu YT, Li BF, and Gao J wrote the manuscript; all of the authors have read and approved the final manuscript.
Supported by the National Natural Science Foundation of China , No. 81571781 .
Institutional review board statement: This study was approved by the Ethics Committee of the Peking University Cancer Hospital, Beijing, China. All patients involved in this study gave their informed consent for participation in the study.
Institutional animal care and use committee statement: The procedures involving the care and use of animals were approved by The Institutional Animal Care and Use Committee of the Peking University.
Conflict-of-interest statement: The authors have no conflicts of interest to declare.
Data sharing statement: The manuscript has no additional data available.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Open-Access: 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/
Corresponding author: Xu Zhu, MD, PhD, Doctor, Professor, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Interventional Therapy, Peking University Cancer Hospital and Institute, No. 52, Fucheng Road, Haidian District, Beijing 100142, China. drzhuxu@163.com
Telephone: +86-10-89196747 Fax: +86-10-89196747
Received: September 28, 2018
Peer-review started: September 28, 2018
First decision: October 23, 2018
Revised: December 25, 2018
Accepted: December 27, 2018
Article in press: December 28, 2018
Published online: February 28, 2019
Peer-review started: September 28, 2018
First decision: October 23, 2018
Revised: December 25, 2018
Accepted: December 27, 2018
Article in press: December 28, 2018
Published online: February 28, 2019
Core Tip
Core tip: Developing brain homeobox 2 (Dbx2) plays an important role in cell differentiation and is frequently upregulated in tumor tissues, while its function in hepatocellular carcinoma (HCC) has not been reported. Our results indicate that Dbx2 is obviously upregulated in HCC tissues and strongly correlated with tumor size. Subsequently, both gain and loss of function assays indicated that Dbx2 promoted HCC migration, invasion, and proliferation by facilitating the transition from G1 to S phase and attenuating apoptosis in vitro and in vivo. Mechanistically, Dbx2 modulates sonic hedgehog signaling by enhancing FTCH1 and GLi1 expression in HCC cells.