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Articles in Press
2/14/2026 7:48:40 AM | Browse: 61 | Download: 0
| Category |
Oncology |
| Manuscript Type |
Basic Study |
| Article Title |
PRMT5 imposed a dual repression on DDIT3 transcription to promote the malignancy of hepatocellular carcinoma
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| Manuscript Source |
Unsolicited Manuscript |
| All Author List |
Hao Jiang, Jin-Hua Yan, Wen-Jing Tang, Bin Shen, Shuai Mo, Yang Wang, De-Hua Hu, Zhi-Xiong Dong and Shu-Bing Zhang |
| Funding Agency and Grant Number |
| Funding Agency |
Grant Number |
| National Natural Science Foundation of China |
No. 82573818 |
| Natural Science Foundation of Hunan Province of China |
No. 2025JJ50542 |
| Key Laboratory of School of Laboratory Medicine and Life Sciences, Wenzhou Medical University |
No. JS2023005 |
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| Corresponding Author |
Shu-Bing Zhang, Manager, Professor, Researcher, Department of Cell Biology, School of Life Sciences, Central South University, No. 172 Tongzipo, Yuelu District, Changsha 410013, Hunan Province, China. shubingzhang@csu.edu.cn |
| Key Words |
Hepatocellular carcinoma; PRMT5; HLCL-61; Apoptosis; Symmetrical dimethylation |
| Core Tip |
High PRMT5 expression was correlated with a worse prognosis of hepatocellular carcinoma (HCC), and inhibition of PRMT5 expression significantly decreased the viability of HCC cells by inducing apoptosis. Mechanistically, PRMT5 dually suppressed the promoter activity of the apoptosis-inducing factor DDIT3 by increasing H4R3me2 modification and recruiting STAT3 to its promoter. The PRMT5 inhibitor HLCL-61 exerted excellent inhibitory efficacy on HCC cells and tissue derived tumors. In general, our study demonstrated that PRMT5 served as an adaptor for STAT3, displaying a dual inhibitory role on DDIT3 transcription to promote apoptosis resistance, and provided that its inhibitor HLCL-61 was an alternative therapeutic approach of HCC. |
| Citation |
Jiang H, Yan JH, Tang WJ, Shen B, Mo S, Wang Y, Hu DH, Dong ZX, Zhang SB. PRMT5 imposed a dual repression on DDIT3 transcription to promote the malignancy of hepatocellular carcinoma. World J Gastroenterol 2026; In press |
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Received |
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2025-10-17 11:31 |
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Peer-Review Started |
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2025-10-17 11:31 |
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First Decision by Editorial Office Director |
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2025-11-19 10:41 |
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Return for Revision |
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2025-11-19 10:41 |
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Revised |
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2025-12-28 13:06 |
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Publication Fee Transferred |
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Second Decision by Editor |
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2026-02-14 02:35 |
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Second Decision by Editor-in-Chief |
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Final Decision by Editorial Office Director |
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2026-02-14 07:48 |
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Articles in Press |
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2026-02-14 07:48 |
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Edit the Manuscript by Language Editor |
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Typeset the Manuscript |
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| ISSN |
1007-9327 (print) and 2219-2840 (online) |
| 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/ |
| Copyright |
© The Author(s) 2026. Published by Baishideng Publishing Group Inc. All rights reserved. |
| Permissions |
For details, please visit: http://www.wjgnet.com/bpg/gerinfo/207
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| Publisher |
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA |
| Website |
http://www.wjgnet.com |
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