Please use this identifier to cite or link to this item: http://hdl.handle.net/11452/30992
Title: Divergent modulation of proteostasis in prostate cancer
Authors: Kırmızıbayrak, Petek Ballar
Gözen, Oğuz
Erzurumlu, Yalçın
Barrio, R
Sutherland, JD
Rodriguez, MS
Bursa Uludağ Üniversitesi/Fen-Edebiyat Fakültesi/Moleküler Biyoloji ve Genetik Bölümü.
Tepedelen, Burcu Erbaykent
CNH-6913-2022
47860936500
Keywords: Biochemistry & molecular biology
Pathology
Research & experimental medicine
Prostate cancer
Ubiquitin
Ubiquitin-like
Deubiquitinase
Autophagy
Unfolded protein response
Unfolded protein response
Androgen receptor-activty
Tumor-suppressor gene
Deubiquitinating enzyme USP12
Ubiquitin ligase SIAH2
Heat-shock proteins
Wild-type spop
Cell-proliferation
Homeobox gene
Transcriptional activity
Issue Date: 10-Apr-2020
Publisher: Springer
Citation: Kırmızıbayrak, P. B. vd. (2020). "Divergent modulation of proteostasis in prostate cancer". ed. R. Barrio vd. Advances in Experimental Medicine and Biology, 1233, 117-151.
Abstract: Proteostasis regulates key cellular processes such as cell proliferation, differentiation, transcription, and apoptosis. The mechanisms by which proteostasis is regulated are crucial and the deterioration of cellular proteostasis has been significantly associated with tumorigenesis since it specifically targets key oncoproteins and tumor suppressors. Prostate cancer (PCa) is the second most common cause of cancer death in men worldwide. Androgens mediate one of the most central signaling pathways in all stages of PCa via the androgen receptor (AR). In addition to their regulation by hormones, PCa cells are also known to be highly secretory and are particularly prone to ER stress as proper ER function is essential. Alterations in various complex signaling pathways and cellular processes including cell cycle control, transcription, DNA repair, apoptosis, cell adhesion, epithelial-mesenchymal transition (EMT), and angiogenesis are critical factors influencing PCa development through key molecular changes mainly by posttranslational modifications in PCa-related proteins, including AR, NKX3.1, PTEN, p53, cyclin D1, and p27. Several ubiquitin ligases like MDM2, Siah2, RNF6, CHIP, and substrate-binding adaptor SPOP; deubiquitinases such as USP7, USP10, USP26, and USP12 are just some of the modifiers involved in the regulation of these key proteins via ubiquitin-proteasome system (UPS). Some ubiquitin-like modifiers, especially SUMOs, have been also closely associated with PCa. On the other hand, the proteotoxicity resulting from misfolded proteins and failure of ER adaptive capacity induce unfolded protein response (UPR) that is an indispensable signaling mechanism for PCa development. Lastly, ER-associated degradation (ERAD) also plays a crucial role in prostate tumorigenesis. In this section, the relationship between prostate cancer and proteostasis will be discussed in terms of UPS, UPR, SUMOylation, ERAD, and autophagy.
URI: https://doi.org/10.1007/978-3-030-38266-7_5
https://link.springer.com/chapter/10.1007/978-3-030-38266-7_5
http://hdl.handle.net/11452/30992
ISBN: 978-3-030-38265-0
978-3-030-38266-7
ISSN: 0065-2598
2214-8019
Appears in Collections:PubMed
Scopus
Web of Science

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