HPV16 <i<E6</i< Oncogene Contributes to Cancer Immune Evasion by Regulating PD-L1 Expression through a miR-143/HIF-1a Pathway

Human Papillomaviruses have been associated with the occurrence of cervical cancer, the fourth most common cancer that affects women globally, while 70% of cases are caused by infection with the high-risk types HPV16 and HPV18. The integration of these viruses’ oncogenes <i<E6</i< and &l...
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Autor*in:	Georgios Konstantopoulos [verfasserIn] Danai Leventakou [verfasserIn] Despoina-Rozi Saltiel [verfasserIn] Efthalia Zervoudi [verfasserIn] Eirini Logotheti [verfasserIn] Spyros Pettas [verfasserIn] Korina Karagianni [verfasserIn] Angeliki Daiou [verfasserIn] Konstantinos E. Hatzistergos [verfasserIn] Dimitra Dafou [verfasserIn] Minas Arsenakis [verfasserIn] Christine Kottaridi [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2024

Schlagwörter:	HPV16 cervical cancer immune escape hypoxia microRNAs E6

Übergeordnetes Werk:	In: Viruses - MDPI AG, 2009, 16(2024), 1, p 113
Übergeordnetes Werk:	volume:16 ; year:2024 ; number:1, p 113

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/v16010113

Katalog-ID:	DOAJ096293993

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allfields	10.3390/v16010113 doi (DE-627)DOAJ096293993 (DE-599)DOAJ43315025fcc44b949ecb430721d050f4 DE-627 ger DE-627 rakwb eng QR1-502 Georgios Konstantopoulos verfasserin aut HPV16 <i<E6</i< Oncogene Contributes to Cancer Immune Evasion by Regulating PD-L1 Expression through a miR-143/HIF-1a Pathway 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Human Papillomaviruses have been associated with the occurrence of cervical cancer, the fourth most common cancer that affects women globally, while 70% of cases are caused by infection with the high-risk types HPV16 and HPV18. The integration of these viruses’ oncogenes <i<E6</i< and <i<E7</i< into the host’s genome affects a multitude of cellular functions and alters the expression of molecules. The aim of this study was to investigate how these oncogenes contribute to the expression of immune system control molecules, using cell lines with integrated HPV16 genome, before and after knocking out <i<E6</i< viral gene using the CRISPR/Cas9 system, delivered with a lentiviral vector. The molecules studied are the T-cell inactivating protein PD-L1, its transcription factor HIF-1a and the latter’s negative regulator, miR-143. According to our results, in the E6 knock out (E6KO) cell lines an increased expression of miR-143 was recorded, while a decrease in the expression of HIF-1a and PD-L1 was exhibited. These findings indicate that E6 protein probably plays a significant role in enabling cervical cancer cells to evade the immune system, while we propose a molecular pathway in cervical cancer, where PD-L1’s expression is regulated by E6 protein through a miR-143/HIF-1a axis. HPV16 cervical cancer immune escape hypoxia microRNAs E6 Microbiology Danai Leventakou verfasserin aut Despoina-Rozi Saltiel verfasserin aut Efthalia Zervoudi verfasserin aut Eirini Logotheti verfasserin aut Spyros Pettas verfasserin aut Korina Karagianni verfasserin aut Angeliki Daiou verfasserin aut Konstantinos E. Hatzistergos verfasserin aut Dimitra Dafou verfasserin aut Minas Arsenakis verfasserin aut Christine Kottaridi verfasserin aut In Viruses MDPI AG, 2009 16(2024), 1, p 113 (DE-627)609775871 (DE-600)2516098-9 19994915 nnns volume:16 year:2024 number:1, p 113 https://doi.org/10.3390/v16010113 kostenfrei https://doaj.org/article/43315025fcc44b949ecb430721d050f4 kostenfrei https://www.mdpi.com/1999-4915/16/1/113 kostenfrei https://doaj.org/toc/1999-4915 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_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_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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 16 2024 1, p 113
spelling	10.3390/v16010113 doi (DE-627)DOAJ096293993 (DE-599)DOAJ43315025fcc44b949ecb430721d050f4 DE-627 ger DE-627 rakwb eng QR1-502 Georgios Konstantopoulos verfasserin aut HPV16 <i<E6</i< Oncogene Contributes to Cancer Immune Evasion by Regulating PD-L1 Expression through a miR-143/HIF-1a Pathway 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Human Papillomaviruses have been associated with the occurrence of cervical cancer, the fourth most common cancer that affects women globally, while 70% of cases are caused by infection with the high-risk types HPV16 and HPV18. The integration of these viruses’ oncogenes <i<E6</i< and <i<E7</i< into the host’s genome affects a multitude of cellular functions and alters the expression of molecules. The aim of this study was to investigate how these oncogenes contribute to the expression of immune system control molecules, using cell lines with integrated HPV16 genome, before and after knocking out <i<E6</i< viral gene using the CRISPR/Cas9 system, delivered with a lentiviral vector. The molecules studied are the T-cell inactivating protein PD-L1, its transcription factor HIF-1a and the latter’s negative regulator, miR-143. According to our results, in the E6 knock out (E6KO) cell lines an increased expression of miR-143 was recorded, while a decrease in the expression of HIF-1a and PD-L1 was exhibited. These findings indicate that E6 protein probably plays a significant role in enabling cervical cancer cells to evade the immune system, while we propose a molecular pathway in cervical cancer, where PD-L1’s expression is regulated by E6 protein through a miR-143/HIF-1a axis. HPV16 cervical cancer immune escape hypoxia microRNAs E6 Microbiology Danai Leventakou verfasserin aut Despoina-Rozi Saltiel verfasserin aut Efthalia Zervoudi verfasserin aut Eirini Logotheti verfasserin aut Spyros Pettas verfasserin aut Korina Karagianni verfasserin aut Angeliki Daiou verfasserin aut Konstantinos E. Hatzistergos verfasserin aut Dimitra Dafou verfasserin aut Minas Arsenakis verfasserin aut Christine Kottaridi verfasserin aut In Viruses MDPI AG, 2009 16(2024), 1, p 113 (DE-627)609775871 (DE-600)2516098-9 19994915 nnns volume:16 year:2024 number:1, p 113 https://doi.org/10.3390/v16010113 kostenfrei https://doaj.org/article/43315025fcc44b949ecb430721d050f4 kostenfrei https://www.mdpi.com/1999-4915/16/1/113 kostenfrei https://doaj.org/toc/1999-4915 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_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_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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 16 2024 1, p 113
allfields_unstemmed	10.3390/v16010113 doi (DE-627)DOAJ096293993 (DE-599)DOAJ43315025fcc44b949ecb430721d050f4 DE-627 ger DE-627 rakwb eng QR1-502 Georgios Konstantopoulos verfasserin aut HPV16 <i<E6</i< Oncogene Contributes to Cancer Immune Evasion by Regulating PD-L1 Expression through a miR-143/HIF-1a Pathway 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Human Papillomaviruses have been associated with the occurrence of cervical cancer, the fourth most common cancer that affects women globally, while 70% of cases are caused by infection with the high-risk types HPV16 and HPV18. The integration of these viruses’ oncogenes <i<E6</i< and <i<E7</i< into the host’s genome affects a multitude of cellular functions and alters the expression of molecules. The aim of this study was to investigate how these oncogenes contribute to the expression of immune system control molecules, using cell lines with integrated HPV16 genome, before and after knocking out <i<E6</i< viral gene using the CRISPR/Cas9 system, delivered with a lentiviral vector. The molecules studied are the T-cell inactivating protein PD-L1, its transcription factor HIF-1a and the latter’s negative regulator, miR-143. According to our results, in the E6 knock out (E6KO) cell lines an increased expression of miR-143 was recorded, while a decrease in the expression of HIF-1a and PD-L1 was exhibited. These findings indicate that E6 protein probably plays a significant role in enabling cervical cancer cells to evade the immune system, while we propose a molecular pathway in cervical cancer, where PD-L1’s expression is regulated by E6 protein through a miR-143/HIF-1a axis. HPV16 cervical cancer immune escape hypoxia microRNAs E6 Microbiology Danai Leventakou verfasserin aut Despoina-Rozi Saltiel verfasserin aut Efthalia Zervoudi verfasserin aut Eirini Logotheti verfasserin aut Spyros Pettas verfasserin aut Korina Karagianni verfasserin aut Angeliki Daiou verfasserin aut Konstantinos E. Hatzistergos verfasserin aut Dimitra Dafou verfasserin aut Minas Arsenakis verfasserin aut Christine Kottaridi verfasserin aut In Viruses MDPI AG, 2009 16(2024), 1, p 113 (DE-627)609775871 (DE-600)2516098-9 19994915 nnns volume:16 year:2024 number:1, p 113 https://doi.org/10.3390/v16010113 kostenfrei https://doaj.org/article/43315025fcc44b949ecb430721d050f4 kostenfrei https://www.mdpi.com/1999-4915/16/1/113 kostenfrei https://doaj.org/toc/1999-4915 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_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_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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 16 2024 1, p 113
allfieldsGer	10.3390/v16010113 doi (DE-627)DOAJ096293993 (DE-599)DOAJ43315025fcc44b949ecb430721d050f4 DE-627 ger DE-627 rakwb eng QR1-502 Georgios Konstantopoulos verfasserin aut HPV16 <i<E6</i< Oncogene Contributes to Cancer Immune Evasion by Regulating PD-L1 Expression through a miR-143/HIF-1a Pathway 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Human Papillomaviruses have been associated with the occurrence of cervical cancer, the fourth most common cancer that affects women globally, while 70% of cases are caused by infection with the high-risk types HPV16 and HPV18. The integration of these viruses’ oncogenes <i<E6</i< and <i<E7</i< into the host’s genome affects a multitude of cellular functions and alters the expression of molecules. The aim of this study was to investigate how these oncogenes contribute to the expression of immune system control molecules, using cell lines with integrated HPV16 genome, before and after knocking out <i<E6</i< viral gene using the CRISPR/Cas9 system, delivered with a lentiviral vector. The molecules studied are the T-cell inactivating protein PD-L1, its transcription factor HIF-1a and the latter’s negative regulator, miR-143. According to our results, in the E6 knock out (E6KO) cell lines an increased expression of miR-143 was recorded, while a decrease in the expression of HIF-1a and PD-L1 was exhibited. These findings indicate that E6 protein probably plays a significant role in enabling cervical cancer cells to evade the immune system, while we propose a molecular pathway in cervical cancer, where PD-L1’s expression is regulated by E6 protein through a miR-143/HIF-1a axis. HPV16 cervical cancer immune escape hypoxia microRNAs E6 Microbiology Danai Leventakou verfasserin aut Despoina-Rozi Saltiel verfasserin aut Efthalia Zervoudi verfasserin aut Eirini Logotheti verfasserin aut Spyros Pettas verfasserin aut Korina Karagianni verfasserin aut Angeliki Daiou verfasserin aut Konstantinos E. Hatzistergos verfasserin aut Dimitra Dafou verfasserin aut Minas Arsenakis verfasserin aut Christine Kottaridi verfasserin aut In Viruses MDPI AG, 2009 16(2024), 1, p 113 (DE-627)609775871 (DE-600)2516098-9 19994915 nnns volume:16 year:2024 number:1, p 113 https://doi.org/10.3390/v16010113 kostenfrei https://doaj.org/article/43315025fcc44b949ecb430721d050f4 kostenfrei https://www.mdpi.com/1999-4915/16/1/113 kostenfrei https://doaj.org/toc/1999-4915 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_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_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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 16 2024 1, p 113
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language	English
source	In Viruses 16(2024), 1, p 113 volume:16 year:2024 number:1, p 113
sourceStr	In Viruses 16(2024), 1, p 113 volume:16 year:2024 number:1, p 113
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	HPV16 cervical cancer immune escape hypoxia microRNAs E6 Microbiology
isfreeaccess_bool	true
container_title	Viruses
authorswithroles_txt_mv	Georgios Konstantopoulos @@aut@@ Danai Leventakou @@aut@@ Despoina-Rozi Saltiel @@aut@@ Efthalia Zervoudi @@aut@@ Eirini Logotheti @@aut@@ Spyros Pettas @@aut@@ Korina Karagianni @@aut@@ Angeliki Daiou @@aut@@ Konstantinos E. Hatzistergos @@aut@@ Dimitra Dafou @@aut@@ Minas Arsenakis @@aut@@ Christine Kottaridi @@aut@@
publishDateDaySort_date	2024-01-01T00:00:00Z
hierarchy_top_id	609775871
id	DOAJ096293993
language_de	englisch
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callnumber-first	Q - Science
author	Georgios Konstantopoulos
spellingShingle	Georgios Konstantopoulos misc QR1-502 misc HPV16 misc cervical cancer misc immune escape misc hypoxia misc microRNAs misc E6 misc Microbiology HPV16 <i<E6</i< Oncogene Contributes to Cancer Immune Evasion by Regulating PD-L1 Expression through a miR-143/HIF-1a Pathway
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topic_title	QR1-502 HPV16 <i<E6</i< Oncogene Contributes to Cancer Immune Evasion by Regulating PD-L1 Expression through a miR-143/HIF-1a Pathway HPV16 cervical cancer immune escape hypoxia microRNAs E6
topic	misc QR1-502 misc HPV16 misc cervical cancer misc immune escape misc hypoxia misc microRNAs misc E6 misc Microbiology
topic_unstemmed	misc QR1-502 misc HPV16 misc cervical cancer misc immune escape misc hypoxia misc microRNAs misc E6 misc Microbiology
topic_browse	misc QR1-502 misc HPV16 misc cervical cancer misc immune escape misc hypoxia misc microRNAs misc E6 misc Microbiology
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title	HPV16 <i<E6</i< Oncogene Contributes to Cancer Immune Evasion by Regulating PD-L1 Expression through a miR-143/HIF-1a Pathway
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title_full	HPV16 <i<E6</i< Oncogene Contributes to Cancer Immune Evasion by Regulating PD-L1 Expression through a miR-143/HIF-1a Pathway
author_sort	Georgios Konstantopoulos
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author_browse	Georgios Konstantopoulos Danai Leventakou Despoina-Rozi Saltiel Efthalia Zervoudi Eirini Logotheti Spyros Pettas Korina Karagianni Angeliki Daiou Konstantinos E. Hatzistergos Dimitra Dafou Minas Arsenakis Christine Kottaridi
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title_sort	hpv16 <i<e6</i< oncogene contributes to cancer immune evasion by regulating pd-l1 expression through a mir-143/hif-1a pathway
callnumber	QR1-502
title_auth	HPV16 <i<E6</i< Oncogene Contributes to Cancer Immune Evasion by Regulating PD-L1 Expression through a miR-143/HIF-1a Pathway
abstract	Human Papillomaviruses have been associated with the occurrence of cervical cancer, the fourth most common cancer that affects women globally, while 70% of cases are caused by infection with the high-risk types HPV16 and HPV18. The integration of these viruses’ oncogenes <i<E6</i< and <i<E7</i< into the host’s genome affects a multitude of cellular functions and alters the expression of molecules. The aim of this study was to investigate how these oncogenes contribute to the expression of immune system control molecules, using cell lines with integrated HPV16 genome, before and after knocking out <i<E6</i< viral gene using the CRISPR/Cas9 system, delivered with a lentiviral vector. The molecules studied are the T-cell inactivating protein PD-L1, its transcription factor HIF-1a and the latter’s negative regulator, miR-143. According to our results, in the E6 knock out (E6KO) cell lines an increased expression of miR-143 was recorded, while a decrease in the expression of HIF-1a and PD-L1 was exhibited. These findings indicate that E6 protein probably plays a significant role in enabling cervical cancer cells to evade the immune system, while we propose a molecular pathway in cervical cancer, where PD-L1’s expression is regulated by E6 protein through a miR-143/HIF-1a axis.
abstractGer	Human Papillomaviruses have been associated with the occurrence of cervical cancer, the fourth most common cancer that affects women globally, while 70% of cases are caused by infection with the high-risk types HPV16 and HPV18. The integration of these viruses’ oncogenes <i<E6</i< and <i<E7</i< into the host’s genome affects a multitude of cellular functions and alters the expression of molecules. The aim of this study was to investigate how these oncogenes contribute to the expression of immune system control molecules, using cell lines with integrated HPV16 genome, before and after knocking out <i<E6</i< viral gene using the CRISPR/Cas9 system, delivered with a lentiviral vector. The molecules studied are the T-cell inactivating protein PD-L1, its transcription factor HIF-1a and the latter’s negative regulator, miR-143. According to our results, in the E6 knock out (E6KO) cell lines an increased expression of miR-143 was recorded, while a decrease in the expression of HIF-1a and PD-L1 was exhibited. These findings indicate that E6 protein probably plays a significant role in enabling cervical cancer cells to evade the immune system, while we propose a molecular pathway in cervical cancer, where PD-L1’s expression is regulated by E6 protein through a miR-143/HIF-1a axis.
abstract_unstemmed	Human Papillomaviruses have been associated with the occurrence of cervical cancer, the fourth most common cancer that affects women globally, while 70% of cases are caused by infection with the high-risk types HPV16 and HPV18. The integration of these viruses’ oncogenes <i<E6</i< and <i<E7</i< into the host’s genome affects a multitude of cellular functions and alters the expression of molecules. The aim of this study was to investigate how these oncogenes contribute to the expression of immune system control molecules, using cell lines with integrated HPV16 genome, before and after knocking out <i<E6</i< viral gene using the CRISPR/Cas9 system, delivered with a lentiviral vector. The molecules studied are the T-cell inactivating protein PD-L1, its transcription factor HIF-1a and the latter’s negative regulator, miR-143. According to our results, in the E6 knock out (E6KO) cell lines an increased expression of miR-143 was recorded, while a decrease in the expression of HIF-1a and PD-L1 was exhibited. These findings indicate that E6 protein probably plays a significant role in enabling cervical cancer cells to evade the immune system, while we propose a molecular pathway in cervical cancer, where PD-L1’s expression is regulated by E6 protein through a miR-143/HIF-1a axis.
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container_issue	1, p 113
title_short	HPV16 <i<E6</i< Oncogene Contributes to Cancer Immune Evasion by Regulating PD-L1 Expression through a miR-143/HIF-1a Pathway
url	https://doi.org/10.3390/v16010113 https://doaj.org/article/43315025fcc44b949ecb430721d050f4 https://www.mdpi.com/1999-4915/16/1/113 https://doaj.org/toc/1999-4915
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author2	Danai Leventakou Despoina-Rozi Saltiel Efthalia Zervoudi Eirini Logotheti Spyros Pettas Korina Karagianni Angeliki Daiou Konstantinos E. Hatzistergos Dimitra Dafou Minas Arsenakis Christine Kottaridi
author2Str	Danai Leventakou Despoina-Rozi Saltiel Efthalia Zervoudi Eirini Logotheti Spyros Pettas Korina Karagianni Angeliki Daiou Konstantinos E. Hatzistergos Dimitra Dafou Minas Arsenakis Christine Kottaridi
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