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YTHDF2 Is a Therapeutic Target for HCC by Suppressing Immune Evasion and Angiogenesis Through ETV5/PD-L1/VEGFA Axis

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收录情况： ◇ SCIE

作者：
Wen Jingyuan[1,2,3] * ; Xue Lin[1,2,3] * ; Wei Yi[1,2,3] * ; Liang Junnan[1,2,3] * ; Jia Wenlong[1,2,3] ; Yong Tuying[4] ; Chu Liang[1,2,3] ; Li Han[1,2,3] ; Han Shenqi[1,2,3] ; Liao Jingyu[1,2,3] ; Chen Zeyu[1,2,3] ; Liu Yiyang[1,2,3] ; Liu Qiumeng[1,2,3] ; Ding Zeyang[1,2,3] ; Liang Huifang[1,2,3] ; Gan Lu[4] ; Chen Xiaoping[1,2,3,5] ; Huang Zhao[1,2,3] ; Zhang Bixiang[1,2,3,5] ;
单位： [1]Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. [2]Clinical Medical Research Center of Hepatic Surgery at Hubei Province, Wuhan, 430030, China. [3]Hubei Key Laboratory of Hepato-Pancreatic-Biliary Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. [4]National Engineering Research Center for Nanomedicine College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, 430074, China. [5]Key Laboratory of Organ Transplantation, Ministry of Education [6]Key Laboratory of Organ Transplantation, National Health Commission [7]Key Laboratory of Organ Transplantation, Chinese Academy of Medical Science, Wuhan, 430030, China.
出处：
DOI： 10.1002/advs.202307242
ISSN：

摘要：
N6-methyladenosine (m6 A) modification orchestrates cancer formation and progression by affecting the tumor microenvironment (TME). For hepatocellular carcinoma (HCC), immune evasion and angiogenesis are characteristic features of its TME. The role of YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), as an m6 A reader, in regulating HCC TME are not fully understood. Herein, it is discovered that trimethylated histone H3 lysine 4 and H3 lysine 27 acetylation modification in the promoter region of YTHDF2 enhanced its expression in HCC, and upregulated YTHDF2 in HCC predicted a worse prognosis. Animal experiments demonstrated that Ythdf2 depletion inhibited spontaneous HCC formation, while its overexpression promoted xenografted HCC progression. Mechanistically, YTHDF2 recognized the m6 A modification in the 5'-untranslational region of ETS variant transcription factor 5 (ETV5) mRNA and recruited eukaryotic translation initiation factor 3 subunit B to facilitate its translation. Elevated ETV5 expression induced the transcription of programmed death ligand-1 and vascular endothelial growth factor A, thereby promoting HCC immune evasion and angiogenesis. Targeting YTHDF2 via small interference RNA-containing aptamer/liposomes successfully both inhibited HCC immune evasion and angiogenesis. Together, this findings reveal the potential application of YTHDF2 in HCC prognosis and targeted treatment.© 2024 The Authors. Advanced Science published by Wiley-VCH GmbH.

基金：
This research was supported by the National Natural Science Foundation of China (82203809, 81372327, 81572427 and 81874189), State Key Project on Infection Disease of China (2018ZX10723204-003-003), National Key Research and Development Program of China (2018YFA0208904), Major Technological Innovation Projects of Hubei Province (2018ACA137), and the Fundamental Research Funds for the Central Universities, HUST (5001540006 and 5001540059).
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出版当年[2023]版：
大类 | 1 区 材料科学
小类 | 1 区 化学：综合 1 区 材料科学：综合 2 区 纳米科技
最新[2025]版：
大类 | 1 区 综合性期刊
小类 | 1 区 化学：综合 1 区 材料科学：综合 1 区 纳米科技
JCR分区：
出版当年[2022]版：
Q1 CHEMISTRY, MULTIDISCIPLINARY Q1 MATERIALS SCIENCE, MULTIDISCIPLINARY Q1 NANOSCIENCE & NANOTECHNOLOGY
最新[2023]版：
Q1 CHEMISTRY, MULTIDISCIPLINARY Q1 MATERIALS SCIENCE, MULTIDISCIPLINARY Q1 NANOSCIENCE & NANOTECHNOLOGY

影响因子： 最新[2023版] 最新五年平均 出版当年[2022版] 出版当年五年平均 出版前一年[2021版] 出版后一年[2023版]

第一作者：
第一作者单位： [1]Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. [2]Clinical Medical Research Center of Hepatic Surgery at Hubei Province, Wuhan, 430030, China. [3]Hubei Key Laboratory of Hepato-Pancreatic-Biliary Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
共同第一作者：
通讯作者：
通讯机构： [1]Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. [2]Clinical Medical Research Center of Hepatic Surgery at Hubei Province, Wuhan, 430030, China. [3]Hubei Key Laboratory of Hepato-Pancreatic-Biliary Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. [5]Key Laboratory of Organ Transplantation, Ministry of Education
推荐引用方式(GB/T 7714)：
Wen Jingyuan,Xue Lin,Wei Yi,et al.YTHDF2 Is a Therapeutic Target for HCC by Suppressing Immune Evasion and Angiogenesis Through ETV5/PD-L1/VEGFA Axis[J].ADVANCED SCIENCE.2024,11(13):e2307242.doi:10.1002/advs.202307242.
APA：
Wen Jingyuan,Xue Lin,Wei Yi,Liang Junnan,Jia Wenlong...&Zhang Bixiang.(2024).YTHDF2 Is a Therapeutic Target for HCC by Suppressing Immune Evasion and Angiogenesis Through ETV5/PD-L1/VEGFA Axis.ADVANCED SCIENCE,11,(13)
MLA：
Wen Jingyuan,et al."YTHDF2 Is a Therapeutic Target for HCC by Suppressing Immune Evasion and Angiogenesis Through ETV5/PD-L1/VEGFA Axis".ADVANCED SCIENCE 11..13(2024):e2307242

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