Prostate cancer cells undergoing ER stress in vitro and in vivo activate transcription of pro-inflammatory cytokines

Navin R Mahadevan, Antonio Fernandez, Jeffrey J Rodvold, Gonzalo Almanza, Maurizio ZanettiThe Laboratory of Immunology, Department of Medicine and Moores Cancer Center, University of California, San Diego, USABackground: Several micro-environmental and cell-intrinsic stimuli cause tumor cells to und...

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Autores principales:	Navin R Mahadevan, Antonio Fernandez, Jeffrey J Rodvold, et al
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2010
Materias:	Pathology RB1-214 Therapeutics. Pharmacology RM1-950
Acceso en línea:	https://doaj.org/article/3201d717df9a454294ba10866f94190a
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spelling	oai:doaj.org-article:3201d717df9a454294ba10866f94190a2021-12-02T05:35:56ZProstate cancer cells undergoing ER stress in vitro and in vivo activate transcription of pro-inflammatory cytokines1178-7031https://doaj.org/article/3201d717df9a454294ba10866f94190a2010-08-01T00:00:00Zhttp://www.dovepress.com/prostate-cancer-cells-undergoing-er-stress-in-vitro-and-in-vivo-activa-a5082https://doaj.org/toc/1178-7031Navin R Mahadevan, Antonio Fernandez, Jeffrey J Rodvold, Gonzalo Almanza, Maurizio ZanettiThe Laboratory of Immunology, Department of Medicine and Moores Cancer Center, University of California, San Diego, USABackground: Several micro-environmental and cell-intrinsic stimuli cause tumor cells to undergo endoplasmic reticulum (ER) stress in vivo. The occurrence of an ER stress response has been associated with tumor progression and angiogenesis. Recently, we found that pharmacological induction of ER stress in B lymphoma cells upregulates the transcription of several pro-inflammatory cytokines.Results: Here, we show that transgenic adenocarcinoma of the mouse prostate (TRAMP) C1 murine prostate cancer cells induced to undergo ER stress in vitro activate the transcription of interleukin 6 (IL-6), interleukin 23p19 (IL-23p19), and tumor necrosis factor a (TNF-a). Furthermore we show that TRAMP C1 tumors growing in vivo spontaneously experience ER stress and that transcription of IL-6, IL-23p19, and TNF-a correlates with the in vivo ER stress response.Conclusions: These results suggest that an ER stress response in prostate cancer cells activates a program of pro-inflammatory cytokine transcription. A possible implication of this finding is that cancer cells may use the ER stress response to modify their microenvironment.Keywords: unfolded protein response, tumorigenesis, inflammation Navin R MahadevanAntonio FernandezJeffrey J Rodvoldet alDove Medical PressarticlePathologyRB1-214Therapeutics. PharmacologyRM1-950ENJournal of Inflammation Research, Vol 2010, Iss default, Pp 99-103 (2010)
institution	DOAJ
collection	DOAJ
language	EN
topic	Pathology RB1-214 Therapeutics. Pharmacology RM1-950
spellingShingle	Pathology RB1-214 Therapeutics. Pharmacology RM1-950 Navin R Mahadevan Antonio Fernandez Jeffrey J Rodvold et al Prostate cancer cells undergoing ER stress in vitro and in vivo activate transcription of pro-inflammatory cytokines
description	Navin R Mahadevan, Antonio Fernandez, Jeffrey J Rodvold, Gonzalo Almanza, Maurizio ZanettiThe Laboratory of Immunology, Department of Medicine and Moores Cancer Center, University of California, San Diego, USABackground: Several micro-environmental and cell-intrinsic stimuli cause tumor cells to undergo endoplasmic reticulum (ER) stress in vivo. The occurrence of an ER stress response has been associated with tumor progression and angiogenesis. Recently, we found that pharmacological induction of ER stress in B lymphoma cells upregulates the transcription of several pro-inflammatory cytokines.Results: Here, we show that transgenic adenocarcinoma of the mouse prostate (TRAMP) C1 murine prostate cancer cells induced to undergo ER stress in vitro activate the transcription of interleukin 6 (IL-6), interleukin 23p19 (IL-23p19), and tumor necrosis factor a (TNF-a). Furthermore we show that TRAMP C1 tumors growing in vivo spontaneously experience ER stress and that transcription of IL-6, IL-23p19, and TNF-a correlates with the in vivo ER stress response.Conclusions: These results suggest that an ER stress response in prostate cancer cells activates a program of pro-inflammatory cytokine transcription. A possible implication of this finding is that cancer cells may use the ER stress response to modify their microenvironment.Keywords: unfolded protein response, tumorigenesis, inflammation
format	article
author	Navin R Mahadevan Antonio Fernandez Jeffrey J Rodvold et al
author_facet	Navin R Mahadevan Antonio Fernandez Jeffrey J Rodvold et al
author_sort	Navin R Mahadevan
title	Prostate cancer cells undergoing ER stress in vitro and in vivo activate transcription of pro-inflammatory cytokines
title_short	Prostate cancer cells undergoing ER stress in vitro and in vivo activate transcription of pro-inflammatory cytokines
title_full	Prostate cancer cells undergoing ER stress in vitro and in vivo activate transcription of pro-inflammatory cytokines
title_fullStr	Prostate cancer cells undergoing ER stress in vitro and in vivo activate transcription of pro-inflammatory cytokines
title_full_unstemmed	Prostate cancer cells undergoing ER stress in vitro and in vivo activate transcription of pro-inflammatory cytokines
title_sort	prostate cancer cells undergoing er stress in vitro and in vivo activate transcription of pro-inflammatory cytokines
publisher	Dove Medical Press
publishDate	2010
url	https://doaj.org/article/3201d717df9a454294ba10866f94190a
work_keys_str_mv	AT navinrmahadevan prostatecancercellsundergoingerstressinvitroandinvivoactivatetranscriptionofproinflammatorycytokines AT antoniofernandez prostatecancercellsundergoingerstressinvitroandinvivoactivatetranscriptionofproinflammatorycytokines AT jeffreyjrodvold prostatecancercellsundergoingerstressinvitroandinvivoactivatetranscriptionofproinflammatorycytokines AT etal prostatecancercellsundergoingerstressinvitroandinvivoactivatetranscriptionofproinflammatorycytokines
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Prostate cancer cells undergoing ER stress in vitro and in vivo activate transcription of pro-inflammatory cytokines

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