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ZEB1: A Critical Regulator of Cell Plasticity, DNA Damage Response, and Therapy Resistance
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SYSNO ASEP 0524939 Druh ASEP J - Článek v odborném periodiku Zařazení RIV J - Článek v odborném periodiku Poddruh J Článek ve WOS Název ZEB1: A Critical Regulator of Cell Plasticity, DNA Damage Response, and Therapy Resistance Tvůrce(i) Drápela, Stanislav (BFU-R) ORCID
Bouchal, J. (CZ)
Jolly, M. K. (IN)
Culig, Z. (CZ)
Souček, Karel (BFU-R) RID, ORCIDCelkový počet autorů 5 Číslo článku 36 Zdroj.dok. Frontiers in molecular biosciences
Roč. 7, MAR 19 2020 (2020)Poč.str. 10 s. Forma vydání Tištěná - P Jazyk dok. eng - angličtina Země vyd. CH - Švýcarsko Klíč. slova epithelial-mesenchymal-transition ; negative breast-cancer ; transcription factor ; drug-resistance ; prostate-cancer Vědní obor RIV CE - Biochemie Obor OECD Biochemistry and molecular biology CEP NV17-28518A GA MZd - Ministerstvo zdravotnictví NV18-08-00245 GA MZd - Ministerstvo zdravotnictví Způsob publikování Open access Institucionální podpora BFU-R - RVO:68081707 UT WOS 000525671300001 EID SCOPUS 85082693724 DOI 10.3389/fmolb.2020.00036 Anotace The predominant way in which conventional chemotherapy kills rapidly proliferating cancer cells is the induction of DNA damage. However, chemoresistance remains the main obstacle to therapy effectivity. An increasing number of studies suggest that epithelial-to-mesenchymal transition (EMT) represents a critical process affecting the sensitivity of cancer cells to chemotherapy. Zinc finger E-box binding homeobox 1 (ZEB1) is a prime element of a network of transcription factors controlling EMT and has been identified as an important molecule in the regulation of DNA damage, cancer cell differentiation, and metastasis. Recent studies have considered upregulation of ZEB1 as a potential modulator of chemoresistance. It has been hypothesized that cancer cells undergoing EMT acquire unique properties that resemble those of cancer stem cells (CSCs). These stem-like cells manifest enhanced DNA damage response (DDR) and DNA repair capacity, self-renewal, or chemoresistance. In contrast, functional experiments have shown that ZEB1 induces chemoresistance regardless of whether other EMT-related changes occur. ZEB1 has also been identified as an important regulator of DDR by the formation of a ZEB1/p300/PCAF complex and direct interaction with ATM kinase, which has been linked to radioresistance. Moreover, ATM can directly phosphorylate ZEB1 and enhance its stability. Downregulation of ZEB1 has also been shown to reduce the abundance of CHK1, an effector kinase of DDR activated by ATR, and to induce its ubiquitin-dependent degradation. In this perspective, we focus on the role of ZEB1 in the regulation of DDR and describe the mechanisms of ZEB1-dependent chemoresistance. Pracoviště Biofyzikální ústav Kontakt Jana Poláková, polakova@ibp.cz, Tel.: 541 517 244 Rok sběru 2021 Elektronická adresa https://apps.webofknowledge.com/full_record.do?product=WOS&search_mode=AdvancedSearch&qid=8&SID=D4ZqAnHn6WSkCM83tcu&page=2&doc=20
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