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Halting hepatocellular carcinoma: Identifying intercellular crosstalk in HBV-driven disease

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资源类型：
Pubmed体系：
作者：
Lingyun Zhou[1] * ; Chang-Hai Liu[1] * ; Duoduo Lv[1] * ; Klarke Michael Sample[1] * ; A ngela Rojas[2,3,4] * ; Yugu Zhang[5] ; Huandi Qiu[6] ; Linye He[7] ; Li Zheng[6] ; Liyu Chen[1] ; Binru Cai[1] ; Yiguo Hu[6,7] ; Manuel Romero-Gomez[2,3,4] ;
机构： [1]Center of Infectious Diseases, West China Hospital of Sichuan University, Chengdu, China [2]SeLiver Group, Institute of Biomedicine of Seville (HUVR/CSIC/US), Department of Medicine, University of Seville, Seville, Spain [3]CIBERehd, Instituto de Salud Carlos III, Madrid, Spain [4]UCM Digestive Diseases, Virgen del Rocı´o University Hospital, Seville, Spain [5]Thoracic Oncology Ward, Cancer Center, and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China [6]State Key Laboratory of Biotherapy and Cancer Center, West China Hospital of Sichuan University, Chengdu, China [7]Thyroid and Parathyroid Surgery Center, West China Hospital of Sichuan University, Chengdu, China
出处：
DOI： 10.1016/j.celrep.2025.115457

摘要：
Hepatitis B infection can lead to liver fibrosis and hepatocellular carcinoma (HCC). Despite antiviral therapies, some patients still develop HCC. This study investigates hepatitis B virus (HBV)-induced hepatocyte-hepatic stellate cell (HSC) crosstalk and its role in liver fibrosis and HCC. Using MYC-driven liver cancer stem cell organoids, HCC-patient-derived xenograft (PDX) models, and HBV replication models, this study reveals that HBV transcription affected hepatocyte development, activated the DNA repair pathway, and promoted glycolysis. HBV activated nicotinamide phosphoribosyltransferase (NAMPT) through DNA damage receptor ATR. NAMPT-insulin receptor (INSR)-mediated hepatocyte-HSC crosstalk caused HSCs to develop a myofibroblast phenotype and activated telomere maintenance mechanisms via PARP1 multisite lactylation. Inhibition of the ATR-NAMPT-INSR-PARP1 pathway effectively blocks HBV-induced liver fibrosis and HCC progression. Targeting this pathway could be a promising strategy for chronic HBV infection management.Copyright © 2025 The Author(s). Published by Elsevier Inc. All rights reserved.

基金：
National Natural Science Foundation of China 81802468 (L. Zhou), Science and Technological Supports Project of Sichuan Province 2023YFS0088 (L.Zhou), Innovate Health Initiative GRIPonMASH project 101132946 (M.R.-G.),Instituto de Salud Carlos III PI22/01342 (M.R.-G.), and Comprehensive AIDS Prevention and Control Research Platform of West China Hospital, Sichuan University 0040204151013 (L.C.).
语种：
外文
PubmedID：
中科院(CAS)分区：
出版当年[2025]版：
大类 | 1 区 生物学
小类 | 2 区 细胞生物学
最新[2025]版：
大类 | 1 区 生物学
小类 | 2 区 细胞生物学
第一作者：
第一作者机构： [1]Center of Infectious Diseases, West China Hospital of Sichuan University, Chengdu, China
共同第一作者：
通讯作者：
通讯机构： [2]SeLiver Group, Institute of Biomedicine of Seville (HUVR/CSIC/US), Department of Medicine, University of Seville, Seville, Spain [3]CIBERehd, Instituto de Salud Carlos III, Madrid, Spain [4]UCM Digestive Diseases, Virgen del Rocı´o University Hospital, Seville, Spain [6]State Key Laboratory of Biotherapy and Cancer Center, West China Hospital of Sichuan University, Chengdu, China [7]Thyroid and Parathyroid Surgery Center, West China Hospital of Sichuan University, Chengdu, China
推荐引用方式(GB/T 7714)：
Lingyun Zhou,Chang-Hai Liu,Duoduo Lv,et al.Halting hepatocellular carcinoma: Identifying intercellular crosstalk in HBV-driven disease[J].Cell Reports.2025,44(4):115457.doi:10.1016/j.celrep.2025.115457.
APA：
Lingyun Zhou,Chang-Hai Liu,Duoduo Lv,Klarke Michael Sample,A ngela Rojas...&Manuel Romero-Gomez.(2025).Halting hepatocellular carcinoma: Identifying intercellular crosstalk in HBV-driven disease.Cell Reports,44,(4)
MLA：
Lingyun Zhou,et al."Halting hepatocellular carcinoma: Identifying intercellular crosstalk in HBV-driven disease".Cell Reports 44..4(2025):115457

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