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CEACAM expression in an in-vitro prostatitis model

BACKGROUND: Prostatitis is an inflammatory disease of the prostate gland, which affects 2-16% of men worldwide and thought to be a cause for prostate cancer (PCa) development. Carcinoembryogenic antigen-related cell adhesion molecules (CEACAMs) are deregulated in inflammation and in PCa. The role of...

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Autores principales: Kube-Golovin, Irina, Lyndin, Mykola, Wiesehöfer, Marc, Wennemuth, Gunther
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10485834/
https://www.ncbi.nlm.nih.gov/pubmed/37691945
http://dx.doi.org/10.3389/fimmu.2023.1236343
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author Kube-Golovin, Irina
Lyndin, Mykola
Wiesehöfer, Marc
Wennemuth, Gunther
author_facet Kube-Golovin, Irina
Lyndin, Mykola
Wiesehöfer, Marc
Wennemuth, Gunther
author_sort Kube-Golovin, Irina
collection PubMed
description BACKGROUND: Prostatitis is an inflammatory disease of the prostate gland, which affects 2-16% of men worldwide and thought to be a cause for prostate cancer (PCa) development. Carcinoembryogenic antigen-related cell adhesion molecules (CEACAMs) are deregulated in inflammation and in PCa. The role of CEACAMs in prostate inflammation and their possible contribution to the malignant transformation of prostate epithelial cells is still elusive. In this study, we investigated the expression of CEACAMs in an in-vitro prostatitis model and their potential role in malignant transformation of prostate epithelial cells. METHODS: Normal prostate epithelial RWPE-1 cells were treated with pro-inflammatory cytokines to achieve an inflammatory state of the cells. The expression of CEACAMs and their related isoforms were analyzed. Additionally, the expression levels of selected CEACAMs were correlated with the expression of malignancy markers and the migratory properties of the cells. RESULTS: This study demonstrates that the pro-inflammatory cytokines, tumor necrosis factor alpha (TNFα) and interferon-gamma (IFNγ), induce synergistically an up-regulation of CEACAM1 expression in RWPE-1 cells, specifically favoring the CEACAM1-L isoform. Furthermore, overexpressed CEACAM1-L is associated with the deregulated expression of JAK/STAT, NFκB, and epithelial-mesenchymal transition (EMT) genes, as well as an increased cell migration. CONCLUSION: We postulate that CEACAM1 isoform CEACAM1-4L may synergistically contribute to inflammation-induced oncogenesis in the prostate.
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spelling pubmed-104858342023-09-09 CEACAM expression in an in-vitro prostatitis model Kube-Golovin, Irina Lyndin, Mykola Wiesehöfer, Marc Wennemuth, Gunther Front Immunol Immunology BACKGROUND: Prostatitis is an inflammatory disease of the prostate gland, which affects 2-16% of men worldwide and thought to be a cause for prostate cancer (PCa) development. Carcinoembryogenic antigen-related cell adhesion molecules (CEACAMs) are deregulated in inflammation and in PCa. The role of CEACAMs in prostate inflammation and their possible contribution to the malignant transformation of prostate epithelial cells is still elusive. In this study, we investigated the expression of CEACAMs in an in-vitro prostatitis model and their potential role in malignant transformation of prostate epithelial cells. METHODS: Normal prostate epithelial RWPE-1 cells were treated with pro-inflammatory cytokines to achieve an inflammatory state of the cells. The expression of CEACAMs and their related isoforms were analyzed. Additionally, the expression levels of selected CEACAMs were correlated with the expression of malignancy markers and the migratory properties of the cells. RESULTS: This study demonstrates that the pro-inflammatory cytokines, tumor necrosis factor alpha (TNFα) and interferon-gamma (IFNγ), induce synergistically an up-regulation of CEACAM1 expression in RWPE-1 cells, specifically favoring the CEACAM1-L isoform. Furthermore, overexpressed CEACAM1-L is associated with the deregulated expression of JAK/STAT, NFκB, and epithelial-mesenchymal transition (EMT) genes, as well as an increased cell migration. CONCLUSION: We postulate that CEACAM1 isoform CEACAM1-4L may synergistically contribute to inflammation-induced oncogenesis in the prostate. Frontiers Media S.A. 2023-08-25 /pmc/articles/PMC10485834/ /pubmed/37691945 http://dx.doi.org/10.3389/fimmu.2023.1236343 Text en Copyright © 2023 Kube-Golovin, Lyndin, Wiesehöfer and Wennemuth https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Kube-Golovin, Irina
Lyndin, Mykola
Wiesehöfer, Marc
Wennemuth, Gunther
CEACAM expression in an in-vitro prostatitis model
title CEACAM expression in an in-vitro prostatitis model
title_full CEACAM expression in an in-vitro prostatitis model
title_fullStr CEACAM expression in an in-vitro prostatitis model
title_full_unstemmed CEACAM expression in an in-vitro prostatitis model
title_short CEACAM expression in an in-vitro prostatitis model
title_sort ceacam expression in an in-vitro prostatitis model
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10485834/
https://www.ncbi.nlm.nih.gov/pubmed/37691945
http://dx.doi.org/10.3389/fimmu.2023.1236343
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