WTAP Accelerates Exhaustion of CD8+ T Cells and Progression of Hepatocellular Carcinoma by Promoting m6A Modification and Translation of PD1 mRNA

The N6-methyladenosine (m6A) methylase WTAP has been identified as a proto-oncogene in multiple cancers, including hepatocellular carcinoma (HCC). Interestingly, although WTAP expression does not differ between normal liver and HCC tissues or across different stages of HCC, patients with higher WTAP...

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Main Authors: Rong Li, Shunle Li, Hua Li, Bingli Liu, Zimu Wang, Huanqin Lei, Yuting Li, Lijuan Jia, Junhui Li, Hongwei Lu, Meng Xu
Format: Article
Language:English
Published: Wiley 2025-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/mi/6217272
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author Rong Li
Shunle Li
Hua Li
Bingli Liu
Zimu Wang
Huanqin Lei
Yuting Li
Lijuan Jia
Junhui Li
Hongwei Lu
Meng Xu
author_facet Rong Li
Shunle Li
Hua Li
Bingli Liu
Zimu Wang
Huanqin Lei
Yuting Li
Lijuan Jia
Junhui Li
Hongwei Lu
Meng Xu
author_sort Rong Li
collection DOAJ
description The N6-methyladenosine (m6A) methylase WTAP has been identified as a proto-oncogene in multiple cancers, including hepatocellular carcinoma (HCC). Interestingly, although WTAP expression does not differ between normal liver and HCC tissues or across different stages of HCC, patients with higher WTAP expression exhibit significantly shorter median survival times (MSTs). Here, we found that WTAP was upregulated in tumor-infiltrating CD8+ T cells, which were more enriched in HCC patients compared to the controls. HCC patients also displayed higher PD1 levels and a greater proportion of exhausted CD8+ T cells (TCF+ PD1+). Moreover, WTAP promoted PD1 expression and suppressed the proliferation and immune activity of CD8+ T cells. In the co-culture system, WTAP-overexpressing CD8+ T cells enhanced the malignancy of HCC cells. Notably, WTAP silencing further augmented the boosting effect of PD1 silencing on CD8+ T cell immune activity and strengthened its inhibitory effect on HCC cell growth. As an m6A “writer”, WTAP increased the m6A level of PD1 mRNA, thereby promoting YTHDF1-mediated translation of PD1. Finally, in the HuNSG xenograft tumor model, WTAP knockdown not only alleviated CD8+ T cell exhaustion and inhibited tumor progression but also synergistically enhanced the antitumor efficacy of anti-PD1 therapy. In conclusion, WTAP promoted CD8+ T cell exhaustion and HCC progression by facilitating the m6A modification and translation of PD1 mRNA.
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spelling doaj-art-916281f36d8e47dfb302d30db86304fa2025-08-20T03:27:07ZengWileyMediators of Inflammation1466-18612025-01-01202510.1155/mi/6217272WTAP Accelerates Exhaustion of CD8+ T Cells and Progression of Hepatocellular Carcinoma by Promoting m6A Modification and Translation of PD1 mRNARong Li0Shunle Li1Hua Li2Bingli Liu3Zimu Wang4Huanqin Lei5Yuting Li6Lijuan Jia7Junhui Li8Hongwei Lu9Meng Xu10Department of AnesthesiologyDepartment of General SurgeryDepartment of General SurgeryDepartment of General SurgeryXi’an Jiaotong University Health Science CenterDepartment of General SurgeryDepartment of General SurgeryDepartment of General SurgeryDepartment of General SurgeryDepartment of General SurgeryDepartment of General SurgeryThe N6-methyladenosine (m6A) methylase WTAP has been identified as a proto-oncogene in multiple cancers, including hepatocellular carcinoma (HCC). Interestingly, although WTAP expression does not differ between normal liver and HCC tissues or across different stages of HCC, patients with higher WTAP expression exhibit significantly shorter median survival times (MSTs). Here, we found that WTAP was upregulated in tumor-infiltrating CD8+ T cells, which were more enriched in HCC patients compared to the controls. HCC patients also displayed higher PD1 levels and a greater proportion of exhausted CD8+ T cells (TCF+ PD1+). Moreover, WTAP promoted PD1 expression and suppressed the proliferation and immune activity of CD8+ T cells. In the co-culture system, WTAP-overexpressing CD8+ T cells enhanced the malignancy of HCC cells. Notably, WTAP silencing further augmented the boosting effect of PD1 silencing on CD8+ T cell immune activity and strengthened its inhibitory effect on HCC cell growth. As an m6A “writer”, WTAP increased the m6A level of PD1 mRNA, thereby promoting YTHDF1-mediated translation of PD1. Finally, in the HuNSG xenograft tumor model, WTAP knockdown not only alleviated CD8+ T cell exhaustion and inhibited tumor progression but also synergistically enhanced the antitumor efficacy of anti-PD1 therapy. In conclusion, WTAP promoted CD8+ T cell exhaustion and HCC progression by facilitating the m6A modification and translation of PD1 mRNA.http://dx.doi.org/10.1155/mi/6217272
spellingShingle Rong Li
Shunle Li
Hua Li
Bingli Liu
Zimu Wang
Huanqin Lei
Yuting Li
Lijuan Jia
Junhui Li
Hongwei Lu
Meng Xu
WTAP Accelerates Exhaustion of CD8+ T Cells and Progression of Hepatocellular Carcinoma by Promoting m6A Modification and Translation of PD1 mRNA
Mediators of Inflammation
title WTAP Accelerates Exhaustion of CD8+ T Cells and Progression of Hepatocellular Carcinoma by Promoting m6A Modification and Translation of PD1 mRNA
title_full WTAP Accelerates Exhaustion of CD8+ T Cells and Progression of Hepatocellular Carcinoma by Promoting m6A Modification and Translation of PD1 mRNA
title_fullStr WTAP Accelerates Exhaustion of CD8+ T Cells and Progression of Hepatocellular Carcinoma by Promoting m6A Modification and Translation of PD1 mRNA
title_full_unstemmed WTAP Accelerates Exhaustion of CD8+ T Cells and Progression of Hepatocellular Carcinoma by Promoting m6A Modification and Translation of PD1 mRNA
title_short WTAP Accelerates Exhaustion of CD8+ T Cells and Progression of Hepatocellular Carcinoma by Promoting m6A Modification and Translation of PD1 mRNA
title_sort wtap accelerates exhaustion of cd8 t cells and progression of hepatocellular carcinoma by promoting m6a modification and translation of pd1 mrna
url http://dx.doi.org/10.1155/mi/6217272
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