CEACAM expression in an in-vitro prostatitis model.

Autor:	Kube-Golovin I; University Hospital Essen, Department of Anatomy, Essen, Germany., Lyndin M; University Hospital Essen, Department of Anatomy, Essen, Germany.; Academic and Research Medical Institute, Department of Pathology, Sumy State University, Sumy, Ukraine., Wiesehöfer M; University Hospital Essen, Department of Anatomy, Essen, Germany., Wennemuth G; University Hospital Essen, Department of Anatomy, Essen, Germany.
Jazyk:	angličtina
Zdroj:	Frontiers in immunology [Front Immunol] 2023 Aug 25; Vol. 14, pp. 1236343. Date of Electronic Publication: 2023 Aug 25 (Print Publication: 2023).
DOI:	10.3389/fimmu.2023.1236343
Abstrakt:	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. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2023 Kube-Golovin, Lyndin, Wiesehöfer and Wennemuth.)
Databáze:	MEDLINE
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