Inactivation of the Tumor Suppressor CYLD Sensitizes Mice to Breast Cancer Development.

Autor:	Pseftogas A; School of Biology, Aristotle University of Thessaloniki, Thessaloniki, Greece., Xanthopoulos K; School of Biology, Aristotle University of Thessaloniki, Thessaloniki, Greece.; School of Pharmacy, Aristotle University of Thessaloniki, Thessaloniki, Greece.; Institute of Applied Biosciences, Centre for Research and Technology, Thessaloniki, Greece., Siasiaridis A; School of Biology, Aristotle University of Thessaloniki, Thessaloniki, Greece., Poutahidis T; School of Veterinary Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece., Gonidas C; School of Biology, Aristotle University of Thessaloniki, Thessaloniki, Greece., Tsingotjidou A; School of Veterinary Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece., Hatzivassiliou E; School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece., Mosialos G; School of Biology, Aristotle University of Thessaloniki, Thessaloniki, Greece; gmosialo@bio.auth.gr.
Jazyk:	angličtina
Zdroj:	Anticancer research [Anticancer Res] 2024 May; Vol. 44 (5), pp. 1885-1894.
DOI:	10.21873/anticanres.16990
Abstrakt:	Background/aim: Breast cancer is a leading cause of cancer-related deaths among women. Down-regulation of the tumor suppressor gene Cyld in breast cancer has been linked to a poor prognosis. This study investigated the role of Cyld in breast cancer using conditional mutant mouse models carrying a Cyld mutation, which inactivates the deubiquitinating activity of its protein product CYLD in mammary epithelial cells. Materials and Methods: We examined the potential of CYLD inactivation to induce mammary tumors spontaneously or modify the susceptibility of mice to mammary tumorigenesis by DMBA treatment or ErbB2 over-expression. Results: CYLD inactivation significantly increased susceptibility to breast cancer induced by either DMBA treatment or ErbB2 over-expression. Moreover, while CYLD inactivation alone did not lead to spontaneous mammary tumorigenesis, it did contribute to the formation of multifocal hyperplastic lesions in virgin mice of predominantly FVB/NJ background. Conclusion: Our study demonstrates the tumor enhancing potential of CYLD inactivation in mammary tumorigenesis in vivo and establishes novel relevant mouse models that can be exploited for developing prognostic and therapeutic protocols. (Copyright © 2024 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)
Databáze:	MEDLINE
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