Basic Study
Copyright ©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastrointest Oncol. Nov 15, 2023; 15(11): 1974-1987
Published online Nov 15, 2023. doi: 10.4251/wjgo.v15.i11.1974
Long non-coding RNA CDKN2B-AS1 promotes hepatocellular carcinoma progression via E2F transcription factor 1/G protein subunit alpha Z axis
Zhi-Gang Tao, Yu-Xiao Yuan, Guo-Wei Wang
Zhi-Gang Tao, Department of Radiology, Hangzhou Cancer Hospital, Hangzhou 310000, Zhejiang Province, China
Yu-Xiao Yuan, Guo-Wei Wang, Department of Radiology, Hangzhou Xixi Hospital, Hangzhou 310012, Zhejiang Province, China
Author contributions: Wang GW conceptualized the study; Tao ZG and Yuan YX performed the experiments, analyzed the data, and drafted the manuscript; and all authors have read and approved the final manuscript.
Institutional review board statement: The study was reviewed and approved by Ethics Committee of Hangzhou Cancer Hospital.
Informed consent statement: The surgical tissues and cells used in this study were not involved in the patients’ privacy information, so the informed consent was waived by the Ethics Committee of Hangzhou Cancer Hospital.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for 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: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Guo-Wei Wang, MD, MM, Attending Doctor, Department of Radiology, Hangzhou Xixi Hospital, No. 2 Hengbu Street, Xihu District, Hangzhou 310012, Zhejiang Province, China. wanguowei6987@126.com
Received: June 23, 2023
Peer-review started: June 23, 2023
First decision: August 30, 2023
Revised: September 12, 2023
Accepted: October 11, 2023
Article in press: October 11, 2023
Published online: November 15, 2023
ARTICLE HIGHLIGHTS
Research background

Long non-coding RNAs (lncRNAs) have been implicated in cancer biology, with lncRNA CDKN2B-AS1 being reported to associate with several human cancers, though its role in hepatocellular carcinoma (HCC) remains unclear.

Research motivation

The motivation behind this research is to better understand the mechanisms underlying the development and progression of HCC, and to explore whether CDKN2B-AS1 could serve as a potential therapeutic target for HCC.

Research objectives

This study aims to investigate the role of the lncRNA CDKN2B-AS1 in HCC progression.

Research methods

This study investigated the role of CDKN2B-AS1 in HCC progression by measuring its expression in HCC using quantitative real-time polymerase chain reaction. Effects on proliferation, cell cycle, and apoptosis of Li-7 and SNU-182 cells were then assessed using the CCK-8 assay, the EdU assay, and flow cytometry. RNA immunoprecipitation was performed to verify the interaction between CDKN2B-AS1 and E2F transcription factor 1 (E2F1). The binding of E2F1 to the promoter of G protein subunit alpha Z (GNAZ) was confirmed using luciferase reporter assay and Chromatin immunoprecipitation. And western blot was utilized to confirm the expression of E2F1 and GNAZ in HCC cells.

Research results

Upregulation of CDKN2B-AS1 was identified in HCC tissues. Inhibited proliferation, induced cell cycle arrest as well as apoptosis were detected in HCC cells with silenced CDKN2B-AS1. In addition, CDKN2B-AS1 was found to interact with E2F1, and its depletion significantly inhibited the binding of E2F1 to the GNAZ promoter region. It has also been found that these effects caused by CDKN2B-AS1 knockdown, can be reversed by E2F1 overexpression.

Research conclusions

In conclusion, the promotion of HCC progression is facilitated by CDKN2B-AS1 recruiting E2F1 to enhance GNAZ transcription.

Research perspectives

This research suggests that CDKN2B-AS1 may serve as a potential therapeutic target for HCC. Further research could investigate the effectiveness of CDKN2B-AS1 inhibition as a treatment for HCC. Additionally, this study provides a better understanding of the mechanisms underlying HCC progression and could inform the development of new diagnostic and treatment approaches for this disease.