CEACAM expression in an in-vitro prostatitis model

BackgroundProstatitis 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 C...

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Main Authors: Irina Kube-Golovin, Mykola Lyndin, Marc Wiesehöfer, Gunther Wennemuth
Format: Article
Language:English
Published: Frontiers Media S.A. 2023-08-01
Series:Frontiers in Immunology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fimmu.2023.1236343/full
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author Irina Kube-Golovin
Mykola Lyndin
Mykola Lyndin
Marc Wiesehöfer
Gunther Wennemuth
author_facet Irina Kube-Golovin
Mykola Lyndin
Mykola Lyndin
Marc Wiesehöfer
Gunther Wennemuth
author_sort Irina Kube-Golovin
collection DOAJ
description BackgroundProstatitis 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.MethodsNormal 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.ResultsThis 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.ConclusionWe postulate that CEACAM1 isoform CEACAM1-4L may synergistically contribute to inflammation-induced oncogenesis in the prostate.
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spelling doaj.art-aee781a8544046ada41c40fee6009caa2023-08-25T18:25:41ZengFrontiers Media S.A.Frontiers in Immunology1664-32242023-08-011410.3389/fimmu.2023.12363431236343CEACAM expression in an in-vitro prostatitis modelIrina Kube-Golovin0Mykola Lyndin1Mykola Lyndin2Marc Wiesehöfer3Gunther Wennemuth4University Hospital Essen, Department of Anatomy, Essen, GermanyUniversity Hospital Essen, Department of Anatomy, Essen, GermanyAcademic and Research Medical Institute, Department of Pathology, Sumy State University, Sumy, UkraineUniversity Hospital Essen, Department of Anatomy, Essen, GermanyUniversity Hospital Essen, Department of Anatomy, Essen, GermanyBackgroundProstatitis 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.MethodsNormal 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.ResultsThis 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.ConclusionWe postulate that CEACAM1 isoform CEACAM1-4L may synergistically contribute to inflammation-induced oncogenesis in the prostate.https://www.frontiersin.org/articles/10.3389/fimmu.2023.1236343/fullprostatitisinflammationCEACAMCEACAM1prostate cancer
spellingShingle Irina Kube-Golovin
Mykola Lyndin
Mykola Lyndin
Marc Wiesehöfer
Gunther Wennemuth
CEACAM expression in an in-vitro prostatitis model
Frontiers in Immunology
prostatitis
inflammation
CEACAM
CEACAM1
prostate cancer
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 prostatitis
inflammation
CEACAM
CEACAM1
prostate cancer
url https://www.frontiersin.org/articles/10.3389/fimmu.2023.1236343/full
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AT marcwiesehofer ceacamexpressioninaninvitroprostatitismodel
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