©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
Dbx2 exhibits a tumor-promoting function in hepatocellular carcinoma cell lines via regulating Shh-Gli1 signaling
Yan-Ting Hu, Bei-Fang Li, Peng-Jun Zhang, Di Wu, Yan-Yan Li, Zhong-Wu Li, Lin Shen, Bin Dong, Jing Gao, Xu Zhu
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.
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
Processing time: 152 Days and 10.9 Hours
ARTICLE HIGHLIGHTS
Research background
Great efforts have been made in exploring the mechanism of hepatocellular carcinoma (HCC), but the details of the HCC pathogenesis are still only partially established. Developing brain homeobox 2 (Dbx2) is frequently upregulated in tumor tissues, while there has been no experimental evidence regarding the function of Dbx2 in HCC.
Research motivation
Investigation of Dbx2 functions may suggest potential molecular mechanisms of hepatocellular carcinogenesis and progression, and further offer the potential for developing novel therapeutic strategies for HCC treatment.
Research objectives
We measured Dbx2 expression in HCC tissues and matched non-tumor tissues and investigated biological functions and the possible molecular mechanisms of Dbx2 in HCC.
Research methods
We detected Dbx2 expression in HCC samples and adjacent non-tumor tissues by immunohistochemistry. The biological behavior of Dbx2 in vitro and in vivo was then assessed by overexpression and knockdown of the Dbx2 gene.
Research results
Dbx2 was upregulated in HCC tissues, which was related to tumor size. Dbx2 had a role of promoting proliferation and metastasis by activating sonic hedgehog (Shh) signaling in HCC.
Research conclusions
Dbx2 was overexpressed in HCC cell lines and tissues, which could promote HCC progression through the Shh signal pathway.
Research perspectives
Dbx2 might serve as a tumor promoter and to be a potential therapeutic target in the future.
