Blocking of EGFR Signaling Is a Latent Strategy for the Improvement of Prognosis of HPV-Induced Cancer

Human papillomavirus (HPV) is a double-stranded DNA (dsDNA) virus, and its high-risk subtypes increase cancer risks. However, the mechanism of HPV infection and pathogenesis still remain unclear. Therefore, understanding the molecular mechanisms and the pathogenesis of HPV are crucial in the prevent...
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Autor*in:	Jianfa Qiu [verfasserIn] Feifei Hu [verfasserIn] Tingting Shao [verfasserIn] Yuqiang Guo [verfasserIn] Zongmao Dai [verfasserIn] Huanhuan Nie [verfasserIn] Oluwatayo Israel Olasunkanmi [verfasserIn] Yue Qi [verfasserIn] Yang Chen [verfasserIn] Lexun Lin [verfasserIn] Wenran Zhao [verfasserIn] Zhaohua Zhong [verfasserIn] Yan Wang [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	EGFR hNSC head and neck squamous cell carcinoma cesC human papillomavirus E7

Übergeordnetes Werk:	In: Frontiers in Oncology - Frontiers Media S.A., 2012, 11(2021)
Übergeordnetes Werk:	volume:11 ; year:2021

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fonc.2021.633794

Katalog-ID:	DOAJ060004320

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520			\|a Human papillomavirus (HPV) is a double-stranded DNA (dsDNA) virus, and its high-risk subtypes increase cancer risks. However, the mechanism of HPV infection and pathogenesis still remain unclear. Therefore, understanding the molecular mechanisms and the pathogenesis of HPV are crucial in the prevention of HPV-related cancers. In this study, we analyzed cervix squamous cell carcinoma (CESC) and head and neck carcinoma (HNSC) combined data to investigate various HPV-induced cancer common features. We showed that epidermal growth factor receptor (EGFR) was downregulated in HPV-positive (HPV+) cancer, and that HPV+ cancer patients exhibited better prognosis than HPV-negative (HPV−) cancer patients. Our study also showed that TP53 mutation rate is lower in HPV+ cancer than in HPV− cancer and that TP53 can be modulated by HPV E7 protein. However, there was no significant difference in the expression of wildtype TP53 in both groups. Subsequently, we constructed HPV-human interaction network and found that EGFR is a critical factor. From the network, we also noticed that EGFR is regulated by HPV E7 protein and hsa-miR-944. Moreover, while phosphorylated EGFR is associated with a worse prognosis, EGFR total express level is not significantly correlated with prognosis. This indicates that EGFR activation will induce a worse outcome in HPV+ cancer patients. Further enrichment analysis showed that EGFR downstream pathway and cancer relative pathway are diversely activated in HPV+ cancer and HPV− cancer. In summary, HPV E7 protein downregulates EGFR that downregulates phosphorylated EGFR and inhibit EGFR-related pathways which in turn and consequently induce better prognosis.
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allfields	10.3389/fonc.2021.633794 doi (DE-627)DOAJ060004320 (DE-599)DOAJc4e201abea3e45a39bcf186f643d6cee DE-627 ger DE-627 rakwb eng RC254-282 Jianfa Qiu verfasserin aut Blocking of EGFR Signaling Is a Latent Strategy for the Improvement of Prognosis of HPV-Induced Cancer 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Human papillomavirus (HPV) is a double-stranded DNA (dsDNA) virus, and its high-risk subtypes increase cancer risks. However, the mechanism of HPV infection and pathogenesis still remain unclear. Therefore, understanding the molecular mechanisms and the pathogenesis of HPV are crucial in the prevention of HPV-related cancers. In this study, we analyzed cervix squamous cell carcinoma (CESC) and head and neck carcinoma (HNSC) combined data to investigate various HPV-induced cancer common features. We showed that epidermal growth factor receptor (EGFR) was downregulated in HPV-positive (HPV+) cancer, and that HPV+ cancer patients exhibited better prognosis than HPV-negative (HPV−) cancer patients. Our study also showed that TP53 mutation rate is lower in HPV+ cancer than in HPV− cancer and that TP53 can be modulated by HPV E7 protein. However, there was no significant difference in the expression of wildtype TP53 in both groups. Subsequently, we constructed HPV-human interaction network and found that EGFR is a critical factor. From the network, we also noticed that EGFR is regulated by HPV E7 protein and hsa-miR-944. Moreover, while phosphorylated EGFR is associated with a worse prognosis, EGFR total express level is not significantly correlated with prognosis. This indicates that EGFR activation will induce a worse outcome in HPV+ cancer patients. Further enrichment analysis showed that EGFR downstream pathway and cancer relative pathway are diversely activated in HPV+ cancer and HPV− cancer. In summary, HPV E7 protein downregulates EGFR that downregulates phosphorylated EGFR and inhibit EGFR-related pathways which in turn and consequently induce better prognosis. EGFR hNSC head and neck squamous cell carcinoma cesC human papillomavirus E7 Neoplasms. Tumors. Oncology. Including cancer and carcinogens Feifei Hu verfasserin aut Tingting Shao verfasserin aut Yuqiang Guo verfasserin aut Zongmao Dai verfasserin aut Huanhuan Nie verfasserin aut Oluwatayo Israel Olasunkanmi verfasserin aut Yue Qi verfasserin aut Yang Chen verfasserin aut Lexun Lin verfasserin aut Wenran Zhao verfasserin aut Zhaohua Zhong verfasserin aut Yan Wang verfasserin aut In Frontiers in Oncology Frontiers Media S.A., 2012 11(2021) (DE-627)684965518 (DE-600)2649216-7 2234943X nnns volume:11 year:2021 https://doi.org/10.3389/fonc.2021.633794 kostenfrei https://doaj.org/article/c4e201abea3e45a39bcf186f643d6cee kostenfrei https://www.frontiersin.org/articles/10.3389/fonc.2021.633794/full kostenfrei https://doaj.org/toc/2234-943X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 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 11 2021
spelling	10.3389/fonc.2021.633794 doi (DE-627)DOAJ060004320 (DE-599)DOAJc4e201abea3e45a39bcf186f643d6cee DE-627 ger DE-627 rakwb eng RC254-282 Jianfa Qiu verfasserin aut Blocking of EGFR Signaling Is a Latent Strategy for the Improvement of Prognosis of HPV-Induced Cancer 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Human papillomavirus (HPV) is a double-stranded DNA (dsDNA) virus, and its high-risk subtypes increase cancer risks. However, the mechanism of HPV infection and pathogenesis still remain unclear. Therefore, understanding the molecular mechanisms and the pathogenesis of HPV are crucial in the prevention of HPV-related cancers. In this study, we analyzed cervix squamous cell carcinoma (CESC) and head and neck carcinoma (HNSC) combined data to investigate various HPV-induced cancer common features. We showed that epidermal growth factor receptor (EGFR) was downregulated in HPV-positive (HPV+) cancer, and that HPV+ cancer patients exhibited better prognosis than HPV-negative (HPV−) cancer patients. Our study also showed that TP53 mutation rate is lower in HPV+ cancer than in HPV− cancer and that TP53 can be modulated by HPV E7 protein. However, there was no significant difference in the expression of wildtype TP53 in both groups. Subsequently, we constructed HPV-human interaction network and found that EGFR is a critical factor. From the network, we also noticed that EGFR is regulated by HPV E7 protein and hsa-miR-944. Moreover, while phosphorylated EGFR is associated with a worse prognosis, EGFR total express level is not significantly correlated with prognosis. This indicates that EGFR activation will induce a worse outcome in HPV+ cancer patients. Further enrichment analysis showed that EGFR downstream pathway and cancer relative pathway are diversely activated in HPV+ cancer and HPV− cancer. In summary, HPV E7 protein downregulates EGFR that downregulates phosphorylated EGFR and inhibit EGFR-related pathways which in turn and consequently induce better prognosis. EGFR hNSC head and neck squamous cell carcinoma cesC human papillomavirus E7 Neoplasms. Tumors. Oncology. Including cancer and carcinogens Feifei Hu verfasserin aut Tingting Shao verfasserin aut Yuqiang Guo verfasserin aut Zongmao Dai verfasserin aut Huanhuan Nie verfasserin aut Oluwatayo Israel Olasunkanmi verfasserin aut Yue Qi verfasserin aut Yang Chen verfasserin aut Lexun Lin verfasserin aut Wenran Zhao verfasserin aut Zhaohua Zhong verfasserin aut Yan Wang verfasserin aut In Frontiers in Oncology Frontiers Media S.A., 2012 11(2021) (DE-627)684965518 (DE-600)2649216-7 2234943X nnns volume:11 year:2021 https://doi.org/10.3389/fonc.2021.633794 kostenfrei https://doaj.org/article/c4e201abea3e45a39bcf186f643d6cee kostenfrei https://www.frontiersin.org/articles/10.3389/fonc.2021.633794/full kostenfrei https://doaj.org/toc/2234-943X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 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 11 2021
allfields_unstemmed	10.3389/fonc.2021.633794 doi (DE-627)DOAJ060004320 (DE-599)DOAJc4e201abea3e45a39bcf186f643d6cee DE-627 ger DE-627 rakwb eng RC254-282 Jianfa Qiu verfasserin aut Blocking of EGFR Signaling Is a Latent Strategy for the Improvement of Prognosis of HPV-Induced Cancer 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Human papillomavirus (HPV) is a double-stranded DNA (dsDNA) virus, and its high-risk subtypes increase cancer risks. However, the mechanism of HPV infection and pathogenesis still remain unclear. Therefore, understanding the molecular mechanisms and the pathogenesis of HPV are crucial in the prevention of HPV-related cancers. In this study, we analyzed cervix squamous cell carcinoma (CESC) and head and neck carcinoma (HNSC) combined data to investigate various HPV-induced cancer common features. We showed that epidermal growth factor receptor (EGFR) was downregulated in HPV-positive (HPV+) cancer, and that HPV+ cancer patients exhibited better prognosis than HPV-negative (HPV−) cancer patients. Our study also showed that TP53 mutation rate is lower in HPV+ cancer than in HPV− cancer and that TP53 can be modulated by HPV E7 protein. However, there was no significant difference in the expression of wildtype TP53 in both groups. Subsequently, we constructed HPV-human interaction network and found that EGFR is a critical factor. From the network, we also noticed that EGFR is regulated by HPV E7 protein and hsa-miR-944. Moreover, while phosphorylated EGFR is associated with a worse prognosis, EGFR total express level is not significantly correlated with prognosis. This indicates that EGFR activation will induce a worse outcome in HPV+ cancer patients. Further enrichment analysis showed that EGFR downstream pathway and cancer relative pathway are diversely activated in HPV+ cancer and HPV− cancer. In summary, HPV E7 protein downregulates EGFR that downregulates phosphorylated EGFR and inhibit EGFR-related pathways which in turn and consequently induce better prognosis. EGFR hNSC head and neck squamous cell carcinoma cesC human papillomavirus E7 Neoplasms. Tumors. Oncology. Including cancer and carcinogens Feifei Hu verfasserin aut Tingting Shao verfasserin aut Yuqiang Guo verfasserin aut Zongmao Dai verfasserin aut Huanhuan Nie verfasserin aut Oluwatayo Israel Olasunkanmi verfasserin aut Yue Qi verfasserin aut Yang Chen verfasserin aut Lexun Lin verfasserin aut Wenran Zhao verfasserin aut Zhaohua Zhong verfasserin aut Yan Wang verfasserin aut In Frontiers in Oncology Frontiers Media S.A., 2012 11(2021) (DE-627)684965518 (DE-600)2649216-7 2234943X nnns volume:11 year:2021 https://doi.org/10.3389/fonc.2021.633794 kostenfrei https://doaj.org/article/c4e201abea3e45a39bcf186f643d6cee kostenfrei https://www.frontiersin.org/articles/10.3389/fonc.2021.633794/full kostenfrei https://doaj.org/toc/2234-943X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 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 11 2021
allfieldsGer	10.3389/fonc.2021.633794 doi (DE-627)DOAJ060004320 (DE-599)DOAJc4e201abea3e45a39bcf186f643d6cee DE-627 ger DE-627 rakwb eng RC254-282 Jianfa Qiu verfasserin aut Blocking of EGFR Signaling Is a Latent Strategy for the Improvement of Prognosis of HPV-Induced Cancer 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Human papillomavirus (HPV) is a double-stranded DNA (dsDNA) virus, and its high-risk subtypes increase cancer risks. However, the mechanism of HPV infection and pathogenesis still remain unclear. Therefore, understanding the molecular mechanisms and the pathogenesis of HPV are crucial in the prevention of HPV-related cancers. In this study, we analyzed cervix squamous cell carcinoma (CESC) and head and neck carcinoma (HNSC) combined data to investigate various HPV-induced cancer common features. We showed that epidermal growth factor receptor (EGFR) was downregulated in HPV-positive (HPV+) cancer, and that HPV+ cancer patients exhibited better prognosis than HPV-negative (HPV−) cancer patients. Our study also showed that TP53 mutation rate is lower in HPV+ cancer than in HPV− cancer and that TP53 can be modulated by HPV E7 protein. However, there was no significant difference in the expression of wildtype TP53 in both groups. Subsequently, we constructed HPV-human interaction network and found that EGFR is a critical factor. From the network, we also noticed that EGFR is regulated by HPV E7 protein and hsa-miR-944. Moreover, while phosphorylated EGFR is associated with a worse prognosis, EGFR total express level is not significantly correlated with prognosis. This indicates that EGFR activation will induce a worse outcome in HPV+ cancer patients. Further enrichment analysis showed that EGFR downstream pathway and cancer relative pathway are diversely activated in HPV+ cancer and HPV− cancer. In summary, HPV E7 protein downregulates EGFR that downregulates phosphorylated EGFR and inhibit EGFR-related pathways which in turn and consequently induce better prognosis. EGFR hNSC head and neck squamous cell carcinoma cesC human papillomavirus E7 Neoplasms. Tumors. Oncology. Including cancer and carcinogens Feifei Hu verfasserin aut Tingting Shao verfasserin aut Yuqiang Guo verfasserin aut Zongmao Dai verfasserin aut Huanhuan Nie verfasserin aut Oluwatayo Israel Olasunkanmi verfasserin aut Yue Qi verfasserin aut Yang Chen verfasserin aut Lexun Lin verfasserin aut Wenran Zhao verfasserin aut Zhaohua Zhong verfasserin aut Yan Wang verfasserin aut In Frontiers in Oncology Frontiers Media S.A., 2012 11(2021) (DE-627)684965518 (DE-600)2649216-7 2234943X nnns volume:11 year:2021 https://doi.org/10.3389/fonc.2021.633794 kostenfrei https://doaj.org/article/c4e201abea3e45a39bcf186f643d6cee kostenfrei https://www.frontiersin.org/articles/10.3389/fonc.2021.633794/full kostenfrei https://doaj.org/toc/2234-943X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 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 11 2021
allfieldsSound	10.3389/fonc.2021.633794 doi (DE-627)DOAJ060004320 (DE-599)DOAJc4e201abea3e45a39bcf186f643d6cee DE-627 ger DE-627 rakwb eng RC254-282 Jianfa Qiu verfasserin aut Blocking of EGFR Signaling Is a Latent Strategy for the Improvement of Prognosis of HPV-Induced Cancer 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Human papillomavirus (HPV) is a double-stranded DNA (dsDNA) virus, and its high-risk subtypes increase cancer risks. However, the mechanism of HPV infection and pathogenesis still remain unclear. Therefore, understanding the molecular mechanisms and the pathogenesis of HPV are crucial in the prevention of HPV-related cancers. In this study, we analyzed cervix squamous cell carcinoma (CESC) and head and neck carcinoma (HNSC) combined data to investigate various HPV-induced cancer common features. We showed that epidermal growth factor receptor (EGFR) was downregulated in HPV-positive (HPV+) cancer, and that HPV+ cancer patients exhibited better prognosis than HPV-negative (HPV−) cancer patients. Our study also showed that TP53 mutation rate is lower in HPV+ cancer than in HPV− cancer and that TP53 can be modulated by HPV E7 protein. However, there was no significant difference in the expression of wildtype TP53 in both groups. Subsequently, we constructed HPV-human interaction network and found that EGFR is a critical factor. From the network, we also noticed that EGFR is regulated by HPV E7 protein and hsa-miR-944. Moreover, while phosphorylated EGFR is associated with a worse prognosis, EGFR total express level is not significantly correlated with prognosis. This indicates that EGFR activation will induce a worse outcome in HPV+ cancer patients. Further enrichment analysis showed that EGFR downstream pathway and cancer relative pathway are diversely activated in HPV+ cancer and HPV− cancer. In summary, HPV E7 protein downregulates EGFR that downregulates phosphorylated EGFR and inhibit EGFR-related pathways which in turn and consequently induce better prognosis. EGFR hNSC head and neck squamous cell carcinoma cesC human papillomavirus E7 Neoplasms. Tumors. Oncology. Including cancer and carcinogens Feifei Hu verfasserin aut Tingting Shao verfasserin aut Yuqiang Guo verfasserin aut Zongmao Dai verfasserin aut Huanhuan Nie verfasserin aut Oluwatayo Israel Olasunkanmi verfasserin aut Yue Qi verfasserin aut Yang Chen verfasserin aut Lexun Lin verfasserin aut Wenran Zhao verfasserin aut Zhaohua Zhong verfasserin aut Yan Wang verfasserin aut In Frontiers in Oncology Frontiers Media S.A., 2012 11(2021) (DE-627)684965518 (DE-600)2649216-7 2234943X nnns volume:11 year:2021 https://doi.org/10.3389/fonc.2021.633794 kostenfrei https://doaj.org/article/c4e201abea3e45a39bcf186f643d6cee kostenfrei https://www.frontiersin.org/articles/10.3389/fonc.2021.633794/full kostenfrei https://doaj.org/toc/2234-943X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 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 11 2021
language	English
source	In Frontiers in Oncology 11(2021) volume:11 year:2021
sourceStr	In Frontiers in Oncology 11(2021) volume:11 year:2021
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	EGFR hNSC head and neck squamous cell carcinoma cesC human papillomavirus E7 Neoplasms. Tumors. Oncology. Including cancer and carcinogens
isfreeaccess_bool	true
container_title	Frontiers in Oncology
authorswithroles_txt_mv	Jianfa Qiu @@aut@@ Feifei Hu @@aut@@ Tingting Shao @@aut@@ Yuqiang Guo @@aut@@ Zongmao Dai @@aut@@ Huanhuan Nie @@aut@@ Oluwatayo Israel Olasunkanmi @@aut@@ Yue Qi @@aut@@ Yang Chen @@aut@@ Lexun Lin @@aut@@ Wenran Zhao @@aut@@ Zhaohua Zhong @@aut@@ Yan Wang @@aut@@
publishDateDaySort_date	2021-01-01T00:00:00Z
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author	Jianfa Qiu
spellingShingle	Jianfa Qiu misc RC254-282 misc EGFR misc hNSC misc head and neck squamous cell carcinoma misc cesC misc human papillomavirus misc E7 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens Blocking of EGFR Signaling Is a Latent Strategy for the Improvement of Prognosis of HPV-Induced Cancer
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topic_title	RC254-282 Blocking of EGFR Signaling Is a Latent Strategy for the Improvement of Prognosis of HPV-Induced Cancer EGFR hNSC head and neck squamous cell carcinoma cesC human papillomavirus E7
topic	misc RC254-282 misc EGFR misc hNSC misc head and neck squamous cell carcinoma misc cesC misc human papillomavirus misc E7 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_unstemmed	misc RC254-282 misc EGFR misc hNSC misc head and neck squamous cell carcinoma misc cesC misc human papillomavirus misc E7 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_browse	misc RC254-282 misc EGFR misc hNSC misc head and neck squamous cell carcinoma misc cesC misc human papillomavirus misc E7 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
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title	Blocking of EGFR Signaling Is a Latent Strategy for the Improvement of Prognosis of HPV-Induced Cancer
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title_full	Blocking of EGFR Signaling Is a Latent Strategy for the Improvement of Prognosis of HPV-Induced Cancer
author_sort	Jianfa Qiu
journal	Frontiers in Oncology
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author_browse	Jianfa Qiu Feifei Hu Tingting Shao Yuqiang Guo Zongmao Dai Huanhuan Nie Oluwatayo Israel Olasunkanmi Yue Qi Yang Chen Lexun Lin Wenran Zhao Zhaohua Zhong Yan Wang
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doi_str_mv	10.3389/fonc.2021.633794
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title_sort	blocking of egfr signaling is a latent strategy for the improvement of prognosis of hpv-induced cancer
callnumber	RC254-282
title_auth	Blocking of EGFR Signaling Is a Latent Strategy for the Improvement of Prognosis of HPV-Induced Cancer
abstract	Human papillomavirus (HPV) is a double-stranded DNA (dsDNA) virus, and its high-risk subtypes increase cancer risks. However, the mechanism of HPV infection and pathogenesis still remain unclear. Therefore, understanding the molecular mechanisms and the pathogenesis of HPV are crucial in the prevention of HPV-related cancers. In this study, we analyzed cervix squamous cell carcinoma (CESC) and head and neck carcinoma (HNSC) combined data to investigate various HPV-induced cancer common features. We showed that epidermal growth factor receptor (EGFR) was downregulated in HPV-positive (HPV+) cancer, and that HPV+ cancer patients exhibited better prognosis than HPV-negative (HPV−) cancer patients. Our study also showed that TP53 mutation rate is lower in HPV+ cancer than in HPV− cancer and that TP53 can be modulated by HPV E7 protein. However, there was no significant difference in the expression of wildtype TP53 in both groups. Subsequently, we constructed HPV-human interaction network and found that EGFR is a critical factor. From the network, we also noticed that EGFR is regulated by HPV E7 protein and hsa-miR-944. Moreover, while phosphorylated EGFR is associated with a worse prognosis, EGFR total express level is not significantly correlated with prognosis. This indicates that EGFR activation will induce a worse outcome in HPV+ cancer patients. Further enrichment analysis showed that EGFR downstream pathway and cancer relative pathway are diversely activated in HPV+ cancer and HPV− cancer. In summary, HPV E7 protein downregulates EGFR that downregulates phosphorylated EGFR and inhibit EGFR-related pathways which in turn and consequently induce better prognosis.
abstractGer	Human papillomavirus (HPV) is a double-stranded DNA (dsDNA) virus, and its high-risk subtypes increase cancer risks. However, the mechanism of HPV infection and pathogenesis still remain unclear. Therefore, understanding the molecular mechanisms and the pathogenesis of HPV are crucial in the prevention of HPV-related cancers. In this study, we analyzed cervix squamous cell carcinoma (CESC) and head and neck carcinoma (HNSC) combined data to investigate various HPV-induced cancer common features. We showed that epidermal growth factor receptor (EGFR) was downregulated in HPV-positive (HPV+) cancer, and that HPV+ cancer patients exhibited better prognosis than HPV-negative (HPV−) cancer patients. Our study also showed that TP53 mutation rate is lower in HPV+ cancer than in HPV− cancer and that TP53 can be modulated by HPV E7 protein. However, there was no significant difference in the expression of wildtype TP53 in both groups. Subsequently, we constructed HPV-human interaction network and found that EGFR is a critical factor. From the network, we also noticed that EGFR is regulated by HPV E7 protein and hsa-miR-944. Moreover, while phosphorylated EGFR is associated with a worse prognosis, EGFR total express level is not significantly correlated with prognosis. This indicates that EGFR activation will induce a worse outcome in HPV+ cancer patients. Further enrichment analysis showed that EGFR downstream pathway and cancer relative pathway are diversely activated in HPV+ cancer and HPV− cancer. In summary, HPV E7 protein downregulates EGFR that downregulates phosphorylated EGFR and inhibit EGFR-related pathways which in turn and consequently induce better prognosis.
abstract_unstemmed	Human papillomavirus (HPV) is a double-stranded DNA (dsDNA) virus, and its high-risk subtypes increase cancer risks. However, the mechanism of HPV infection and pathogenesis still remain unclear. Therefore, understanding the molecular mechanisms and the pathogenesis of HPV are crucial in the prevention of HPV-related cancers. In this study, we analyzed cervix squamous cell carcinoma (CESC) and head and neck carcinoma (HNSC) combined data to investigate various HPV-induced cancer common features. We showed that epidermal growth factor receptor (EGFR) was downregulated in HPV-positive (HPV+) cancer, and that HPV+ cancer patients exhibited better prognosis than HPV-negative (HPV−) cancer patients. Our study also showed that TP53 mutation rate is lower in HPV+ cancer than in HPV− cancer and that TP53 can be modulated by HPV E7 protein. However, there was no significant difference in the expression of wildtype TP53 in both groups. Subsequently, we constructed HPV-human interaction network and found that EGFR is a critical factor. From the network, we also noticed that EGFR is regulated by HPV E7 protein and hsa-miR-944. Moreover, while phosphorylated EGFR is associated with a worse prognosis, EGFR total express level is not significantly correlated with prognosis. This indicates that EGFR activation will induce a worse outcome in HPV+ cancer patients. Further enrichment analysis showed that EGFR downstream pathway and cancer relative pathway are diversely activated in HPV+ cancer and HPV− cancer. In summary, HPV E7 protein downregulates EGFR that downregulates phosphorylated EGFR and inhibit EGFR-related pathways which in turn and consequently induce better prognosis.
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title_short	Blocking of EGFR Signaling Is a Latent Strategy for the Improvement of Prognosis of HPV-Induced Cancer
url	https://doi.org/10.3389/fonc.2021.633794 https://doaj.org/article/c4e201abea3e45a39bcf186f643d6cee https://www.frontiersin.org/articles/10.3389/fonc.2021.633794/full https://doaj.org/toc/2234-943X
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author2	Feifei Hu Tingting Shao Yuqiang Guo Zongmao Dai Huanhuan Nie Oluwatayo Israel Olasunkanmi Yue Qi Yang Chen Lexun Lin Wenran Zhao Zhaohua Zhong Yan Wang
author2Str	Feifei Hu Tingting Shao Yuqiang Guo Zongmao Dai Huanhuan Nie Oluwatayo Israel Olasunkanmi Yue Qi Yang Chen Lexun Lin Wenran Zhao Zhaohua Zhong Yan Wang
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up_date	2024-07-04T01:42:09.227Z
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