YTHDF2 Is a Therapeutic Target for HCC by Suppressing Immune Evasion and Angiogenesis Through ETV5/PD‐L1/VEGFA Axis
Abstract N6‐methyladenosine (m6A) 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 prote...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Jingyuan Wen [verfasserIn] Lin Xue [verfasserIn] Yi Wei [verfasserIn] Junnan Liang [verfasserIn] Wenlong Jia [verfasserIn] Tuying Yong [verfasserIn] Liang Chu [verfasserIn] Han Li [verfasserIn] Shenqi Han [verfasserIn] Jingyu Liao [verfasserIn] Zeyu Chen [verfasserIn] Yiyang Liu [verfasserIn] Qiumeng Liu [verfasserIn] Zeyang Ding [verfasserIn] Huifang Liang [verfasserIn] Lu Gan [verfasserIn] Xiaoping Chen [verfasserIn] Zhao Huang [verfasserIn] Bixiang Zhang [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2024 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
In: Advanced Science - Wiley, 2015, 11(2024), 13, Seite n/a-n/a |
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| Übergeordnetes Werk: |
volume:11 ; year:2024 ; number:13 ; pages:n/a-n/a |
| Links: |
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| DOI / URN: |
10.1002/advs.202307242 |
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| Katalog-ID: |
DOAJ091417058 |
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| 245 | 1 | 0 | |a YTHDF2 Is a Therapeutic Target for HCC by Suppressing Immune Evasion and Angiogenesis Through ETV5/PD‐L1/VEGFA Axis |
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| 520 | |a Abstract N6‐methyladenosine (m6A) 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 m6A 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 m6A 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. | ||
| 650 | 4 | |a angiogenesis | |
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| 650 | 4 | |a ETV5 | |
| 650 | 4 | |a immune evasion | |
| 650 | 4 | |a Liver cancer | |
| 650 | 4 | |a N6‐methyladenosine | |
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| 700 | 0 | |a Wenlong Jia |e verfasserin |4 aut | |
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| 700 | 0 | |a Shenqi Han |e verfasserin |4 aut | |
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| 700 | 0 | |a Qiumeng Liu |e verfasserin |4 aut | |
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| 700 | 0 | |a Huifang Liang |e verfasserin |4 aut | |
| 700 | 0 | |a Lu Gan |e verfasserin |4 aut | |
| 700 | 0 | |a Xiaoping Chen |e verfasserin |4 aut | |
| 700 | 0 | |a Zhao Huang |e verfasserin |4 aut | |
| 700 | 0 | |a Bixiang Zhang |e verfasserin |4 aut | |
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10.1002/advs.202307242 doi (DE-627)DOAJ091417058 (DE-599)DOAJ032662a368f74c4c88369259157f4c3d DE-627 ger DE-627 rakwb eng Jingyuan Wen verfasserin aut YTHDF2 Is a Therapeutic Target for HCC by Suppressing Immune Evasion and Angiogenesis Through ETV5/PD‐L1/VEGFA Axis 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract N6‐methyladenosine (m6A) 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 m6A 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 m6A 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. angiogenesis eIF3b ETV5 immune evasion Liver cancer N6‐methyladenosine Science Q Lin Xue verfasserin aut Yi Wei verfasserin aut Junnan Liang verfasserin aut Wenlong Jia verfasserin aut Tuying Yong verfasserin aut Liang Chu verfasserin aut Han Li verfasserin aut Shenqi Han verfasserin aut Jingyu Liao verfasserin aut Zeyu Chen verfasserin aut Yiyang Liu verfasserin aut Qiumeng Liu verfasserin aut Zeyang Ding verfasserin aut Huifang Liang verfasserin aut Lu Gan verfasserin aut Xiaoping Chen verfasserin aut Zhao Huang verfasserin aut Bixiang Zhang verfasserin aut In Advanced Science Wiley, 2015 11(2024), 13, Seite n/a-n/a (DE-627)817357777 (DE-600)2808093-2 21983844 nnns volume:11 year:2024 number:13 pages:n/a-n/a https://doi.org/10.1002/advs.202307242 kostenfrei https://doaj.org/article/032662a368f74c4c88369259157f4c3d kostenfrei https://doi.org/10.1002/advs.202307242 kostenfrei https://doaj.org/toc/2198-3844 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2024 13 n/a-n/a |
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10.1002/advs.202307242 doi (DE-627)DOAJ091417058 (DE-599)DOAJ032662a368f74c4c88369259157f4c3d DE-627 ger DE-627 rakwb eng Jingyuan Wen verfasserin aut YTHDF2 Is a Therapeutic Target for HCC by Suppressing Immune Evasion and Angiogenesis Through ETV5/PD‐L1/VEGFA Axis 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract N6‐methyladenosine (m6A) 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 m6A 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 m6A 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. angiogenesis eIF3b ETV5 immune evasion Liver cancer N6‐methyladenosine Science Q Lin Xue verfasserin aut Yi Wei verfasserin aut Junnan Liang verfasserin aut Wenlong Jia verfasserin aut Tuying Yong verfasserin aut Liang Chu verfasserin aut Han Li verfasserin aut Shenqi Han verfasserin aut Jingyu Liao verfasserin aut Zeyu Chen verfasserin aut Yiyang Liu verfasserin aut Qiumeng Liu verfasserin aut Zeyang Ding verfasserin aut Huifang Liang verfasserin aut Lu Gan verfasserin aut Xiaoping Chen verfasserin aut Zhao Huang verfasserin aut Bixiang Zhang verfasserin aut In Advanced Science Wiley, 2015 11(2024), 13, Seite n/a-n/a (DE-627)817357777 (DE-600)2808093-2 21983844 nnns volume:11 year:2024 number:13 pages:n/a-n/a https://doi.org/10.1002/advs.202307242 kostenfrei https://doaj.org/article/032662a368f74c4c88369259157f4c3d kostenfrei https://doi.org/10.1002/advs.202307242 kostenfrei https://doaj.org/toc/2198-3844 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2024 13 n/a-n/a |
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10.1002/advs.202307242 doi (DE-627)DOAJ091417058 (DE-599)DOAJ032662a368f74c4c88369259157f4c3d DE-627 ger DE-627 rakwb eng Jingyuan Wen verfasserin aut YTHDF2 Is a Therapeutic Target for HCC by Suppressing Immune Evasion and Angiogenesis Through ETV5/PD‐L1/VEGFA Axis 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract N6‐methyladenosine (m6A) 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 m6A 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 m6A 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. angiogenesis eIF3b ETV5 immune evasion Liver cancer N6‐methyladenosine Science Q Lin Xue verfasserin aut Yi Wei verfasserin aut Junnan Liang verfasserin aut Wenlong Jia verfasserin aut Tuying Yong verfasserin aut Liang Chu verfasserin aut Han Li verfasserin aut Shenqi Han verfasserin aut Jingyu Liao verfasserin aut Zeyu Chen verfasserin aut Yiyang Liu verfasserin aut Qiumeng Liu verfasserin aut Zeyang Ding verfasserin aut Huifang Liang verfasserin aut Lu Gan verfasserin aut Xiaoping Chen verfasserin aut Zhao Huang verfasserin aut Bixiang Zhang verfasserin aut In Advanced Science Wiley, 2015 11(2024), 13, Seite n/a-n/a (DE-627)817357777 (DE-600)2808093-2 21983844 nnns volume:11 year:2024 number:13 pages:n/a-n/a https://doi.org/10.1002/advs.202307242 kostenfrei https://doaj.org/article/032662a368f74c4c88369259157f4c3d kostenfrei https://doi.org/10.1002/advs.202307242 kostenfrei https://doaj.org/toc/2198-3844 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2024 13 n/a-n/a |
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10.1002/advs.202307242 doi (DE-627)DOAJ091417058 (DE-599)DOAJ032662a368f74c4c88369259157f4c3d DE-627 ger DE-627 rakwb eng Jingyuan Wen verfasserin aut YTHDF2 Is a Therapeutic Target for HCC by Suppressing Immune Evasion and Angiogenesis Through ETV5/PD‐L1/VEGFA Axis 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract N6‐methyladenosine (m6A) 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 m6A 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 m6A 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. angiogenesis eIF3b ETV5 immune evasion Liver cancer N6‐methyladenosine Science Q Lin Xue verfasserin aut Yi Wei verfasserin aut Junnan Liang verfasserin aut Wenlong Jia verfasserin aut Tuying Yong verfasserin aut Liang Chu verfasserin aut Han Li verfasserin aut Shenqi Han verfasserin aut Jingyu Liao verfasserin aut Zeyu Chen verfasserin aut Yiyang Liu verfasserin aut Qiumeng Liu verfasserin aut Zeyang Ding verfasserin aut Huifang Liang verfasserin aut Lu Gan verfasserin aut Xiaoping Chen verfasserin aut Zhao Huang verfasserin aut Bixiang Zhang verfasserin aut In Advanced Science Wiley, 2015 11(2024), 13, Seite n/a-n/a (DE-627)817357777 (DE-600)2808093-2 21983844 nnns volume:11 year:2024 number:13 pages:n/a-n/a https://doi.org/10.1002/advs.202307242 kostenfrei https://doaj.org/article/032662a368f74c4c88369259157f4c3d kostenfrei https://doi.org/10.1002/advs.202307242 kostenfrei https://doaj.org/toc/2198-3844 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2024 13 n/a-n/a |
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10.1002/advs.202307242 doi (DE-627)DOAJ091417058 (DE-599)DOAJ032662a368f74c4c88369259157f4c3d DE-627 ger DE-627 rakwb eng Jingyuan Wen verfasserin aut YTHDF2 Is a Therapeutic Target for HCC by Suppressing Immune Evasion and Angiogenesis Through ETV5/PD‐L1/VEGFA Axis 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract N6‐methyladenosine (m6A) 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 m6A 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 m6A 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. angiogenesis eIF3b ETV5 immune evasion Liver cancer N6‐methyladenosine Science Q Lin Xue verfasserin aut Yi Wei verfasserin aut Junnan Liang verfasserin aut Wenlong Jia verfasserin aut Tuying Yong verfasserin aut Liang Chu verfasserin aut Han Li verfasserin aut Shenqi Han verfasserin aut Jingyu Liao verfasserin aut Zeyu Chen verfasserin aut Yiyang Liu verfasserin aut Qiumeng Liu verfasserin aut Zeyang Ding verfasserin aut Huifang Liang verfasserin aut Lu Gan verfasserin aut Xiaoping Chen verfasserin aut Zhao Huang verfasserin aut Bixiang Zhang verfasserin aut In Advanced Science Wiley, 2015 11(2024), 13, Seite n/a-n/a (DE-627)817357777 (DE-600)2808093-2 21983844 nnns volume:11 year:2024 number:13 pages:n/a-n/a https://doi.org/10.1002/advs.202307242 kostenfrei https://doaj.org/article/032662a368f74c4c88369259157f4c3d kostenfrei https://doi.org/10.1002/advs.202307242 kostenfrei https://doaj.org/toc/2198-3844 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2024 13 n/a-n/a |
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Jingyuan Wen @@aut@@ Lin Xue @@aut@@ Yi Wei @@aut@@ Junnan Liang @@aut@@ Wenlong Jia @@aut@@ Tuying Yong @@aut@@ Liang Chu @@aut@@ Han Li @@aut@@ Shenqi Han @@aut@@ Jingyu Liao @@aut@@ Zeyu Chen @@aut@@ Yiyang Liu @@aut@@ Qiumeng Liu @@aut@@ Zeyang Ding @@aut@@ Huifang Liang @@aut@@ Lu Gan @@aut@@ Xiaoping Chen @@aut@@ Zhao Huang @@aut@@ Bixiang Zhang @@aut@@ |
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| author |
Jingyuan Wen |
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Jingyuan Wen misc angiogenesis misc eIF3b misc ETV5 misc immune evasion misc Liver cancer misc N6‐methyladenosine misc Science misc Q YTHDF2 Is a Therapeutic Target for HCC by Suppressing Immune Evasion and Angiogenesis Through ETV5/PD‐L1/VEGFA Axis |
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YTHDF2 Is a Therapeutic Target for HCC by Suppressing Immune Evasion and Angiogenesis Through ETV5/PD‐L1/VEGFA Axis angiogenesis eIF3b ETV5 immune evasion Liver cancer N6‐methyladenosine |
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misc angiogenesis misc eIF3b misc ETV5 misc immune evasion misc Liver cancer misc N6‐methyladenosine misc Science misc Q |
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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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YTHDF2 Is a Therapeutic Target for HCC by Suppressing Immune Evasion and Angiogenesis Through ETV5/PD‐L1/VEGFA Axis |
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Jingyuan Wen Lin Xue Yi Wei Junnan Liang Wenlong Jia Tuying Yong Liang Chu Han Li Shenqi Han Jingyu Liao Zeyu Chen Yiyang Liu Qiumeng Liu Zeyang Ding Huifang Liang Lu Gan Xiaoping Chen Zhao Huang Bixiang Zhang |
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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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YTHDF2 Is a Therapeutic Target for HCC by Suppressing Immune Evasion and Angiogenesis Through ETV5/PD‐L1/VEGFA Axis |
| abstract |
Abstract N6‐methyladenosine (m6A) 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 m6A 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 m6A 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. |
| abstractGer |
Abstract N6‐methyladenosine (m6A) 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 m6A 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 m6A 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. |
| abstract_unstemmed |
Abstract N6‐methyladenosine (m6A) 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 m6A 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 m6A 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. |
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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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https://doi.org/10.1002/advs.202307242 https://doaj.org/article/032662a368f74c4c88369259157f4c3d https://doaj.org/toc/2198-3844 |
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Lin Xue Yi Wei Junnan Liang Wenlong Jia Tuying Yong Liang Chu Han Li Shenqi Han Jingyu Liao Zeyu Chen Yiyang Liu Qiumeng Liu Zeyang Ding Huifang Liang Lu Gan Xiaoping Chen Zhao Huang Bixiang Zhang |
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Lin Xue Yi Wei Junnan Liang Wenlong Jia Tuying Yong Liang Chu Han Li Shenqi Han Jingyu Liao Zeyu Chen Yiyang Liu Qiumeng Liu Zeyang Ding Huifang Liang Lu Gan Xiaoping Chen Zhao Huang Bixiang Zhang |
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10.1002/advs.202307242 |
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2024-07-03T20:16:40.143Z |
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