DHX34 deficiency triggers tumor-intrinsic immunity via a dsRNA-mediated type I interferon pathway activation in HCC

Tumors often evade immune surveillance by crippling their immunogenicity in the microenvironment. DHX34, an RNA helicase involved in nonsense-mediated mRNA decay pathway, is critical for aberrant RNA degradation. However, the effect of DHX34 in regulating the immunogenicity in hepatocellular carcino...

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Main Authors: Chunli Zhang, Limin Huang, Zeyu Li, Qian Wang, Nanbin Liu, Chongyu Zhang, Xi Liu, Chen Zhang, Gaixia He, Jin Sun, Zongfang Li, Hongwei Tian
Format: Article
Language:English
Published: Elsevier 2025-09-01
Series:Neoplasia: An International Journal for Oncology Research
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Online Access:http://www.sciencedirect.com/science/article/pii/S1476558625000788
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author Chunli Zhang
Limin Huang
Zeyu Li
Qian Wang
Nanbin Liu
Chongyu Zhang
Xi Liu
Chen Zhang
Gaixia He
Jin Sun
Zongfang Li
Hongwei Tian
author_facet Chunli Zhang
Limin Huang
Zeyu Li
Qian Wang
Nanbin Liu
Chongyu Zhang
Xi Liu
Chen Zhang
Gaixia He
Jin Sun
Zongfang Li
Hongwei Tian
author_sort Chunli Zhang
collection DOAJ
description Tumors often evade immune surveillance by crippling their immunogenicity in the microenvironment. DHX34, an RNA helicase involved in nonsense-mediated mRNA decay pathway, is critical for aberrant RNA degradation. However, the effect of DHX34 in regulating the immunogenicity in hepatocellular carcinoma (HCC) is still unclear. Here, a surprising function of DHX34 in inhibited HCC immunogenicity is identified. DHX34-deficient tumors were infiltrated by activated T cells that impaired tumor growth and enhanced survival in mice. Mechanistically, DHX34 depletion triggered dsRNA accumulation which may activate cytosolic RNA-sensing pathway effectors such as MAVS, p-IKK, p-IRF3, and the subsequent type-I interferon response, evoking tumor-intrinsic immunity and leading to CD8 T activation. Collectively, DHX34 is implicated as a regulator that orchestrates a barrier in HCC by suppressing dsRNA-driven innate immune activation. Targeting DHX34 may enhance tumor immunogenicity and synergize with immunotherapies, offering a novel therapeutic strategy for HCC.
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issn 1476-5586
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publishDate 2025-09-01
publisher Elsevier
record_format Article
series Neoplasia: An International Journal for Oncology Research
spelling doaj-art-53e95024d6c841f497e8ef930136ef2e2025-08-20T03:09:14ZengElsevierNeoplasia: An International Journal for Oncology Research1476-55862025-09-016710119810.1016/j.neo.2025.101198DHX34 deficiency triggers tumor-intrinsic immunity via a dsRNA-mediated type I interferon pathway activation in HCCChunli Zhang0Limin Huang1Zeyu Li2Qian Wang3Nanbin Liu4Chongyu Zhang5Xi Liu6Chen Zhang7Gaixia He8Jin Sun9Zongfang Li10Hongwei Tian11Department of General Surgery, National-Local Joint Engineering Research Center of Biodiagnostic & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, PR ChinaDepartment of General Surgery, National-Local Joint Engineering Research Center of Biodiagnostic & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, PR ChinaDepartment of General Surgery, National-Local Joint Engineering Research Center of Biodiagnostic & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, PR ChinaDepartment of Tumor and Immunology in Precision Medical Institute, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi, PR ChinaDepartment of General Surgery, National-Local Joint Engineering Research Center of Biodiagnostic & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, PR ChinaDepartment of General Surgery, National-Local Joint Engineering Research Center of Biodiagnostic & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, PR ChinaDepartment of General Surgery, National-Local Joint Engineering Research Center of Biodiagnostic & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, PR ChinaDepartment of General Surgery, National-Local Joint Engineering Research Center of Biodiagnostic & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, PR ChinaDepartment of General Surgery, National-Local Joint Engineering Research Center of Biodiagnostic & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, PR China; Shaanxi Provincial Clinical Medical Research Center for Liver and Spleen Diseases, CHESS-Shaanxi consortium, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, PR ChinaDepartment of General Surgery, National-Local Joint Engineering Research Center of Biodiagnostic & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, PR China; Department of Tumor and Immunology in Precision Medical Institute, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi, PR ChinaDepartment of General Surgery, National-Local Joint Engineering Research Center of Biodiagnostic & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, PR China; Department of Tumor and Immunology in Precision Medical Institute, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi, PR China; Shaanxi Provincial Clinical Medical Research Center for Liver and Spleen Diseases, CHESS-Shaanxi consortium, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, PR China; Key Laboratory of Environment and Genes Related to Diseases, Xi’an Jiaotong University, Ministry of Education of China, Shaanxi, PR China; Corresponding authors at: National and Local Joint Engineering Research Center of Biodiagnosis and Biotherapy, The Second Affiliated Hospital of Xi’an Jiaotong University, 71004 Xi’an, PR China.Department of General Surgery, National-Local Joint Engineering Research Center of Biodiagnostic & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, PR China; Department of Tumor and Immunology in Precision Medical Institute, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi, PR China; Corresponding authors at: National and Local Joint Engineering Research Center of Biodiagnosis and Biotherapy, The Second Affiliated Hospital of Xi’an Jiaotong University, 71004 Xi’an, PR China.Tumors often evade immune surveillance by crippling their immunogenicity in the microenvironment. DHX34, an RNA helicase involved in nonsense-mediated mRNA decay pathway, is critical for aberrant RNA degradation. However, the effect of DHX34 in regulating the immunogenicity in hepatocellular carcinoma (HCC) is still unclear. Here, a surprising function of DHX34 in inhibited HCC immunogenicity is identified. DHX34-deficient tumors were infiltrated by activated T cells that impaired tumor growth and enhanced survival in mice. Mechanistically, DHX34 depletion triggered dsRNA accumulation which may activate cytosolic RNA-sensing pathway effectors such as MAVS, p-IKK, p-IRF3, and the subsequent type-I interferon response, evoking tumor-intrinsic immunity and leading to CD8 T activation. Collectively, DHX34 is implicated as a regulator that orchestrates a barrier in HCC by suppressing dsRNA-driven innate immune activation. Targeting DHX34 may enhance tumor immunogenicity and synergize with immunotherapies, offering a novel therapeutic strategy for HCC.http://www.sciencedirect.com/science/article/pii/S1476558625000788DHX34Hepatocellular carcinomadsRNAImmune evasionType I interferon
spellingShingle Chunli Zhang
Limin Huang
Zeyu Li
Qian Wang
Nanbin Liu
Chongyu Zhang
Xi Liu
Chen Zhang
Gaixia He
Jin Sun
Zongfang Li
Hongwei Tian
DHX34 deficiency triggers tumor-intrinsic immunity via a dsRNA-mediated type I interferon pathway activation in HCC
Neoplasia: An International Journal for Oncology Research
DHX34
Hepatocellular carcinoma
dsRNA
Immune evasion
Type I interferon
title DHX34 deficiency triggers tumor-intrinsic immunity via a dsRNA-mediated type I interferon pathway activation in HCC
title_full DHX34 deficiency triggers tumor-intrinsic immunity via a dsRNA-mediated type I interferon pathway activation in HCC
title_fullStr DHX34 deficiency triggers tumor-intrinsic immunity via a dsRNA-mediated type I interferon pathway activation in HCC
title_full_unstemmed DHX34 deficiency triggers tumor-intrinsic immunity via a dsRNA-mediated type I interferon pathway activation in HCC
title_short DHX34 deficiency triggers tumor-intrinsic immunity via a dsRNA-mediated type I interferon pathway activation in HCC
title_sort dhx34 deficiency triggers tumor intrinsic immunity via a dsrna mediated type i interferon pathway activation in hcc
topic DHX34
Hepatocellular carcinoma
dsRNA
Immune evasion
Type I interferon
url http://www.sciencedirect.com/science/article/pii/S1476558625000788
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