HIF-1α Mediates Immunosuppression and Chemoresistance in Colorectal Cancer by Inhibiting CXCL9, −10 and −11

Uncertainty exists regarding the mechanisms by which hypoxia-inducible factors (HIFs) control CD8+T-cell migration into tumor microenvironments. Here, we found that HIF-1α knockdown or overexpression resulted in increased or decreased CXCL9, −10, and −11 expression in vitro, respectively. Gene Set V...
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Autor*in:	Yixi Su [verfasserIn] Jiaqi Liu [verfasserIn] Yu Tian [verfasserIn] Haiyan Dong [verfasserIn] Mengchen Shi [verfasserIn] Jingdan Zhang [verfasserIn] Weiqian Li [verfasserIn] Qiang Huang [verfasserIn] Nanlin Xiang [verfasserIn] Chen Wang [verfasserIn] Jun Liu [verfasserIn] Lingyuan He [verfasserIn] Limei Hu [verfasserIn] Ann M. Haberman [verfasserIn] Huanliang Liu [verfasserIn] Xiangling Yang [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2024

Schlagwörter:	HIF-1α BIRC2 CXCL9 CXCL10 CXCL11 CD8+ T Cell

Übergeordnetes Werk:	In: Biomedicine & Pharmacotherapy - Elsevier, 2021, 173(2024), Seite 116427-
Übergeordnetes Werk:	volume:173 ; year:2024 ; pages:116427-

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.biopha.2024.116427

Katalog-ID:	DOAJ095783032

Internformat


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allfields	10.1016/j.biopha.2024.116427 doi (DE-627)DOAJ095783032 (DE-599)DOAJ4dd5ea43925b41b09e9fb42862b38bf5 DE-627 ger DE-627 rakwb eng RM1-950 Yixi Su verfasserin aut HIF-1α Mediates Immunosuppression and Chemoresistance in Colorectal Cancer by Inhibiting CXCL9, −10 and −11 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Uncertainty exists regarding the mechanisms by which hypoxia-inducible factors (HIFs) control CD8+T-cell migration into tumor microenvironments. Here, we found that HIF-1α knockdown or overexpression resulted in increased or decreased CXCL9, −10, and −11 expression in vitro, respectively. Gene Set Variation Analysis revealed that elevated HIF-1α levels correlated with a poor prognosis, severe pathological stage, and an absence of CD8+ T cells in the tumor microenvironment in colorectal cancer (CRC) patients. HIF-1α was inversely associated with pathways beneficial to anti-tumor immunotherapy and cytokine/chemokine function. In vivo, inhibiting HIF-1α or its upstream regulator BIRC2 significantly suppressed tumor growth and promoted CD8+ T-cell infiltration. CXCR3 neutralizing antibodies reversed these effects, implicating the involvement of CXCL9, −10, and −11/CXCR3 axis. The presence of HIF-1α weakened the upregulation of CXCL9, −10, and −11 by bleomycin and doxorubicin. Combining HIF-1α inhibition with bleomycin promoted CD8+ T-cell infiltration and tumor suppression in vivo. Moreover, doxorubicin could upregulate CXCL9, −10 and −11 by suppressing HIF-1α. Our findings highlight the potential of HIF-1α inhibition to improve CRC microenvironments and increase chemotherapy sensitivity. HIF-1α BIRC2 CXCL9 CXCL10 CXCL11 CD8+ T Cell Therapeutics. Pharmacology Jiaqi Liu verfasserin aut Yu Tian verfasserin aut Haiyan Dong verfasserin aut Mengchen Shi verfasserin aut Jingdan Zhang verfasserin aut Weiqian Li verfasserin aut Qiang Huang verfasserin aut Nanlin Xiang verfasserin aut Chen Wang verfasserin aut Jun Liu verfasserin aut Lingyuan He verfasserin aut Limei Hu verfasserin aut Ann M. Haberman verfasserin aut Huanliang Liu verfasserin aut Xiangling Yang verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 173(2024), Seite 116427- (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:173 year:2024 pages:116427- https://doi.org/10.1016/j.biopha.2024.116427 kostenfrei https://doaj.org/article/4dd5ea43925b41b09e9fb42862b38bf5 kostenfrei http://www.sciencedirect.com/science/article/pii/S0753332224003111 kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 173 2024 116427-
spelling	10.1016/j.biopha.2024.116427 doi (DE-627)DOAJ095783032 (DE-599)DOAJ4dd5ea43925b41b09e9fb42862b38bf5 DE-627 ger DE-627 rakwb eng RM1-950 Yixi Su verfasserin aut HIF-1α Mediates Immunosuppression and Chemoresistance in Colorectal Cancer by Inhibiting CXCL9, −10 and −11 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Uncertainty exists regarding the mechanisms by which hypoxia-inducible factors (HIFs) control CD8+T-cell migration into tumor microenvironments. Here, we found that HIF-1α knockdown or overexpression resulted in increased or decreased CXCL9, −10, and −11 expression in vitro, respectively. Gene Set Variation Analysis revealed that elevated HIF-1α levels correlated with a poor prognosis, severe pathological stage, and an absence of CD8+ T cells in the tumor microenvironment in colorectal cancer (CRC) patients. HIF-1α was inversely associated with pathways beneficial to anti-tumor immunotherapy and cytokine/chemokine function. In vivo, inhibiting HIF-1α or its upstream regulator BIRC2 significantly suppressed tumor growth and promoted CD8+ T-cell infiltration. CXCR3 neutralizing antibodies reversed these effects, implicating the involvement of CXCL9, −10, and −11/CXCR3 axis. The presence of HIF-1α weakened the upregulation of CXCL9, −10, and −11 by bleomycin and doxorubicin. Combining HIF-1α inhibition with bleomycin promoted CD8+ T-cell infiltration and tumor suppression in vivo. Moreover, doxorubicin could upregulate CXCL9, −10 and −11 by suppressing HIF-1α. Our findings highlight the potential of HIF-1α inhibition to improve CRC microenvironments and increase chemotherapy sensitivity. HIF-1α BIRC2 CXCL9 CXCL10 CXCL11 CD8+ T Cell Therapeutics. Pharmacology Jiaqi Liu verfasserin aut Yu Tian verfasserin aut Haiyan Dong verfasserin aut Mengchen Shi verfasserin aut Jingdan Zhang verfasserin aut Weiqian Li verfasserin aut Qiang Huang verfasserin aut Nanlin Xiang verfasserin aut Chen Wang verfasserin aut Jun Liu verfasserin aut Lingyuan He verfasserin aut Limei Hu verfasserin aut Ann M. Haberman verfasserin aut Huanliang Liu verfasserin aut Xiangling Yang verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 173(2024), Seite 116427- (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:173 year:2024 pages:116427- https://doi.org/10.1016/j.biopha.2024.116427 kostenfrei https://doaj.org/article/4dd5ea43925b41b09e9fb42862b38bf5 kostenfrei http://www.sciencedirect.com/science/article/pii/S0753332224003111 kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 173 2024 116427-
allfields_unstemmed	10.1016/j.biopha.2024.116427 doi (DE-627)DOAJ095783032 (DE-599)DOAJ4dd5ea43925b41b09e9fb42862b38bf5 DE-627 ger DE-627 rakwb eng RM1-950 Yixi Su verfasserin aut HIF-1α Mediates Immunosuppression and Chemoresistance in Colorectal Cancer by Inhibiting CXCL9, −10 and −11 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Uncertainty exists regarding the mechanisms by which hypoxia-inducible factors (HIFs) control CD8+T-cell migration into tumor microenvironments. Here, we found that HIF-1α knockdown or overexpression resulted in increased or decreased CXCL9, −10, and −11 expression in vitro, respectively. Gene Set Variation Analysis revealed that elevated HIF-1α levels correlated with a poor prognosis, severe pathological stage, and an absence of CD8+ T cells in the tumor microenvironment in colorectal cancer (CRC) patients. HIF-1α was inversely associated with pathways beneficial to anti-tumor immunotherapy and cytokine/chemokine function. In vivo, inhibiting HIF-1α or its upstream regulator BIRC2 significantly suppressed tumor growth and promoted CD8+ T-cell infiltration. CXCR3 neutralizing antibodies reversed these effects, implicating the involvement of CXCL9, −10, and −11/CXCR3 axis. The presence of HIF-1α weakened the upregulation of CXCL9, −10, and −11 by bleomycin and doxorubicin. Combining HIF-1α inhibition with bleomycin promoted CD8+ T-cell infiltration and tumor suppression in vivo. Moreover, doxorubicin could upregulate CXCL9, −10 and −11 by suppressing HIF-1α. Our findings highlight the potential of HIF-1α inhibition to improve CRC microenvironments and increase chemotherapy sensitivity. HIF-1α BIRC2 CXCL9 CXCL10 CXCL11 CD8+ T Cell Therapeutics. Pharmacology Jiaqi Liu verfasserin aut Yu Tian verfasserin aut Haiyan Dong verfasserin aut Mengchen Shi verfasserin aut Jingdan Zhang verfasserin aut Weiqian Li verfasserin aut Qiang Huang verfasserin aut Nanlin Xiang verfasserin aut Chen Wang verfasserin aut Jun Liu verfasserin aut Lingyuan He verfasserin aut Limei Hu verfasserin aut Ann M. Haberman verfasserin aut Huanliang Liu verfasserin aut Xiangling Yang verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 173(2024), Seite 116427- (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:173 year:2024 pages:116427- https://doi.org/10.1016/j.biopha.2024.116427 kostenfrei https://doaj.org/article/4dd5ea43925b41b09e9fb42862b38bf5 kostenfrei http://www.sciencedirect.com/science/article/pii/S0753332224003111 kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 173 2024 116427-
allfieldsGer	10.1016/j.biopha.2024.116427 doi (DE-627)DOAJ095783032 (DE-599)DOAJ4dd5ea43925b41b09e9fb42862b38bf5 DE-627 ger DE-627 rakwb eng RM1-950 Yixi Su verfasserin aut HIF-1α Mediates Immunosuppression and Chemoresistance in Colorectal Cancer by Inhibiting CXCL9, −10 and −11 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Uncertainty exists regarding the mechanisms by which hypoxia-inducible factors (HIFs) control CD8+T-cell migration into tumor microenvironments. Here, we found that HIF-1α knockdown or overexpression resulted in increased or decreased CXCL9, −10, and −11 expression in vitro, respectively. Gene Set Variation Analysis revealed that elevated HIF-1α levels correlated with a poor prognosis, severe pathological stage, and an absence of CD8+ T cells in the tumor microenvironment in colorectal cancer (CRC) patients. HIF-1α was inversely associated with pathways beneficial to anti-tumor immunotherapy and cytokine/chemokine function. In vivo, inhibiting HIF-1α or its upstream regulator BIRC2 significantly suppressed tumor growth and promoted CD8+ T-cell infiltration. CXCR3 neutralizing antibodies reversed these effects, implicating the involvement of CXCL9, −10, and −11/CXCR3 axis. The presence of HIF-1α weakened the upregulation of CXCL9, −10, and −11 by bleomycin and doxorubicin. Combining HIF-1α inhibition with bleomycin promoted CD8+ T-cell infiltration and tumor suppression in vivo. Moreover, doxorubicin could upregulate CXCL9, −10 and −11 by suppressing HIF-1α. Our findings highlight the potential of HIF-1α inhibition to improve CRC microenvironments and increase chemotherapy sensitivity. HIF-1α BIRC2 CXCL9 CXCL10 CXCL11 CD8+ T Cell Therapeutics. Pharmacology Jiaqi Liu verfasserin aut Yu Tian verfasserin aut Haiyan Dong verfasserin aut Mengchen Shi verfasserin aut Jingdan Zhang verfasserin aut Weiqian Li verfasserin aut Qiang Huang verfasserin aut Nanlin Xiang verfasserin aut Chen Wang verfasserin aut Jun Liu verfasserin aut Lingyuan He verfasserin aut Limei Hu verfasserin aut Ann M. Haberman verfasserin aut Huanliang Liu verfasserin aut Xiangling Yang verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 173(2024), Seite 116427- (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:173 year:2024 pages:116427- https://doi.org/10.1016/j.biopha.2024.116427 kostenfrei https://doaj.org/article/4dd5ea43925b41b09e9fb42862b38bf5 kostenfrei http://www.sciencedirect.com/science/article/pii/S0753332224003111 kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 173 2024 116427-
allfieldsSound	10.1016/j.biopha.2024.116427 doi (DE-627)DOAJ095783032 (DE-599)DOAJ4dd5ea43925b41b09e9fb42862b38bf5 DE-627 ger DE-627 rakwb eng RM1-950 Yixi Su verfasserin aut HIF-1α Mediates Immunosuppression and Chemoresistance in Colorectal Cancer by Inhibiting CXCL9, −10 and −11 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Uncertainty exists regarding the mechanisms by which hypoxia-inducible factors (HIFs) control CD8+T-cell migration into tumor microenvironments. Here, we found that HIF-1α knockdown or overexpression resulted in increased or decreased CXCL9, −10, and −11 expression in vitro, respectively. Gene Set Variation Analysis revealed that elevated HIF-1α levels correlated with a poor prognosis, severe pathological stage, and an absence of CD8+ T cells in the tumor microenvironment in colorectal cancer (CRC) patients. HIF-1α was inversely associated with pathways beneficial to anti-tumor immunotherapy and cytokine/chemokine function. In vivo, inhibiting HIF-1α or its upstream regulator BIRC2 significantly suppressed tumor growth and promoted CD8+ T-cell infiltration. CXCR3 neutralizing antibodies reversed these effects, implicating the involvement of CXCL9, −10, and −11/CXCR3 axis. The presence of HIF-1α weakened the upregulation of CXCL9, −10, and −11 by bleomycin and doxorubicin. Combining HIF-1α inhibition with bleomycin promoted CD8+ T-cell infiltration and tumor suppression in vivo. Moreover, doxorubicin could upregulate CXCL9, −10 and −11 by suppressing HIF-1α. Our findings highlight the potential of HIF-1α inhibition to improve CRC microenvironments and increase chemotherapy sensitivity. HIF-1α BIRC2 CXCL9 CXCL10 CXCL11 CD8+ T Cell Therapeutics. Pharmacology Jiaqi Liu verfasserin aut Yu Tian verfasserin aut Haiyan Dong verfasserin aut Mengchen Shi verfasserin aut Jingdan Zhang verfasserin aut Weiqian Li verfasserin aut Qiang Huang verfasserin aut Nanlin Xiang verfasserin aut Chen Wang verfasserin aut Jun Liu verfasserin aut Lingyuan He verfasserin aut Limei Hu verfasserin aut Ann M. Haberman verfasserin aut Huanliang Liu verfasserin aut Xiangling Yang verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 173(2024), Seite 116427- (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:173 year:2024 pages:116427- https://doi.org/10.1016/j.biopha.2024.116427 kostenfrei https://doaj.org/article/4dd5ea43925b41b09e9fb42862b38bf5 kostenfrei http://www.sciencedirect.com/science/article/pii/S0753332224003111 kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 173 2024 116427-
language	English
source	In Biomedicine & Pharmacotherapy 173(2024), Seite 116427- volume:173 year:2024 pages:116427-
sourceStr	In Biomedicine & Pharmacotherapy 173(2024), Seite 116427- volume:173 year:2024 pages:116427-
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	HIF-1α BIRC2 CXCL9 CXCL10 CXCL11 CD8+ T Cell Therapeutics. Pharmacology
isfreeaccess_bool	true
container_title	Biomedicine & Pharmacotherapy
authorswithroles_txt_mv	Yixi Su @@aut@@ Jiaqi Liu @@aut@@ Yu Tian @@aut@@ Haiyan Dong @@aut@@ Mengchen Shi @@aut@@ Jingdan Zhang @@aut@@ Weiqian Li @@aut@@ Qiang Huang @@aut@@ Nanlin Xiang @@aut@@ Chen Wang @@aut@@ Jun Liu @@aut@@ Lingyuan He @@aut@@ Limei Hu @@aut@@ Ann M. Haberman @@aut@@ Huanliang Liu @@aut@@ Xiangling Yang @@aut@@
publishDateDaySort_date	2024-01-01T00:00:00Z
hierarchy_top_id	306717565
id	DOAJ095783032
language_de	englisch
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callnumber-first	R - Medicine
author	Yixi Su
spellingShingle	Yixi Su misc RM1-950 misc HIF-1α misc BIRC2 misc CXCL9 misc CXCL10 misc CXCL11 misc CD8+ T Cell misc Therapeutics. Pharmacology HIF-1α Mediates Immunosuppression and Chemoresistance in Colorectal Cancer by Inhibiting CXCL9, −10 and −11
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topic_title	RM1-950 HIF-1α Mediates Immunosuppression and Chemoresistance in Colorectal Cancer by Inhibiting CXCL9, −10 and −11 HIF-1α BIRC2 CXCL9 CXCL10 CXCL11 CD8+ T Cell
topic	misc RM1-950 misc HIF-1α misc BIRC2 misc CXCL9 misc CXCL10 misc CXCL11 misc CD8+ T Cell misc Therapeutics. Pharmacology
topic_unstemmed	misc RM1-950 misc HIF-1α misc BIRC2 misc CXCL9 misc CXCL10 misc CXCL11 misc CD8+ T Cell misc Therapeutics. Pharmacology
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title	HIF-1α Mediates Immunosuppression and Chemoresistance in Colorectal Cancer by Inhibiting CXCL9, −10 and −11
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title_full	HIF-1α Mediates Immunosuppression and Chemoresistance in Colorectal Cancer by Inhibiting CXCL9, −10 and −11
author_sort	Yixi Su
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author_browse	Yixi Su Jiaqi Liu Yu Tian Haiyan Dong Mengchen Shi Jingdan Zhang Weiqian Li Qiang Huang Nanlin Xiang Chen Wang Jun Liu Lingyuan He Limei Hu Ann M. Haberman Huanliang Liu Xiangling Yang
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title_sort	hif-1α mediates immunosuppression and chemoresistance in colorectal cancer by inhibiting cxcl9, −10 and −11
callnumber	RM1-950
title_auth	HIF-1α Mediates Immunosuppression and Chemoresistance in Colorectal Cancer by Inhibiting CXCL9, −10 and −11
abstract	Uncertainty exists regarding the mechanisms by which hypoxia-inducible factors (HIFs) control CD8+T-cell migration into tumor microenvironments. Here, we found that HIF-1α knockdown or overexpression resulted in increased or decreased CXCL9, −10, and −11 expression in vitro, respectively. Gene Set Variation Analysis revealed that elevated HIF-1α levels correlated with a poor prognosis, severe pathological stage, and an absence of CD8+ T cells in the tumor microenvironment in colorectal cancer (CRC) patients. HIF-1α was inversely associated with pathways beneficial to anti-tumor immunotherapy and cytokine/chemokine function. In vivo, inhibiting HIF-1α or its upstream regulator BIRC2 significantly suppressed tumor growth and promoted CD8+ T-cell infiltration. CXCR3 neutralizing antibodies reversed these effects, implicating the involvement of CXCL9, −10, and −11/CXCR3 axis. The presence of HIF-1α weakened the upregulation of CXCL9, −10, and −11 by bleomycin and doxorubicin. Combining HIF-1α inhibition with bleomycin promoted CD8+ T-cell infiltration and tumor suppression in vivo. Moreover, doxorubicin could upregulate CXCL9, −10 and −11 by suppressing HIF-1α. Our findings highlight the potential of HIF-1α inhibition to improve CRC microenvironments and increase chemotherapy sensitivity.
abstractGer	Uncertainty exists regarding the mechanisms by which hypoxia-inducible factors (HIFs) control CD8+T-cell migration into tumor microenvironments. Here, we found that HIF-1α knockdown or overexpression resulted in increased or decreased CXCL9, −10, and −11 expression in vitro, respectively. Gene Set Variation Analysis revealed that elevated HIF-1α levels correlated with a poor prognosis, severe pathological stage, and an absence of CD8+ T cells in the tumor microenvironment in colorectal cancer (CRC) patients. HIF-1α was inversely associated with pathways beneficial to anti-tumor immunotherapy and cytokine/chemokine function. In vivo, inhibiting HIF-1α or its upstream regulator BIRC2 significantly suppressed tumor growth and promoted CD8+ T-cell infiltration. CXCR3 neutralizing antibodies reversed these effects, implicating the involvement of CXCL9, −10, and −11/CXCR3 axis. The presence of HIF-1α weakened the upregulation of CXCL9, −10, and −11 by bleomycin and doxorubicin. Combining HIF-1α inhibition with bleomycin promoted CD8+ T-cell infiltration and tumor suppression in vivo. Moreover, doxorubicin could upregulate CXCL9, −10 and −11 by suppressing HIF-1α. Our findings highlight the potential of HIF-1α inhibition to improve CRC microenvironments and increase chemotherapy sensitivity.
abstract_unstemmed	Uncertainty exists regarding the mechanisms by which hypoxia-inducible factors (HIFs) control CD8+T-cell migration into tumor microenvironments. Here, we found that HIF-1α knockdown or overexpression resulted in increased or decreased CXCL9, −10, and −11 expression in vitro, respectively. Gene Set Variation Analysis revealed that elevated HIF-1α levels correlated with a poor prognosis, severe pathological stage, and an absence of CD8+ T cells in the tumor microenvironment in colorectal cancer (CRC) patients. HIF-1α was inversely associated with pathways beneficial to anti-tumor immunotherapy and cytokine/chemokine function. In vivo, inhibiting HIF-1α or its upstream regulator BIRC2 significantly suppressed tumor growth and promoted CD8+ T-cell infiltration. CXCR3 neutralizing antibodies reversed these effects, implicating the involvement of CXCL9, −10, and −11/CXCR3 axis. The presence of HIF-1α weakened the upregulation of CXCL9, −10, and −11 by bleomycin and doxorubicin. Combining HIF-1α inhibition with bleomycin promoted CD8+ T-cell infiltration and tumor suppression in vivo. Moreover, doxorubicin could upregulate CXCL9, −10 and −11 by suppressing HIF-1α. Our findings highlight the potential of HIF-1α inhibition to improve CRC microenvironments and increase chemotherapy sensitivity.
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title_short	HIF-1α Mediates Immunosuppression and Chemoresistance in Colorectal Cancer by Inhibiting CXCL9, −10 and −11
url	https://doi.org/10.1016/j.biopha.2024.116427 https://doaj.org/article/4dd5ea43925b41b09e9fb42862b38bf5 http://www.sciencedirect.com/science/article/pii/S0753332224003111 https://doaj.org/toc/0753-3322
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HIF-1α Mediates Immunosuppression and Chemoresistance in Colorectal Cancer by Inhibiting CXCL9, −10 and −11

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