ID | 61723 |
FullText URL | |
Author |
Bi, Zhuoyue
Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University
Zhang, Qian
Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University
Fu, Yao
Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University
Seno, Akimasa
Faculty of Engineering, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
ORCID
Kaken ID
publons
researchmap
Wadgaonkar, Priya
Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University
Qiu, Yiran
Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University
Almutairy, Bandar
Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University
Xu, Liping
Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University
Zhang, Wenxuan
Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University
Thakur, Chitra
Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University
Chen, Fei
Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University
|
Abstract | Environmental exposure to arsenic, a well-established carcinogen linked to a number of human cancers, is a public health concern in many areas of the world. Despite extensive studies on the molecular mechanisms of arsenic-induced carcinogenesis, how initial cellular responses, such as activation of stress kinases and the generation of reactive oxygen species, converge to affect the transcriptional and/or epigenetic reprogramming required for the malignant transformation of normal cells or normal stem cells remains to be elucidated. In this review, we discuss some recent discoveries showing how the transcription factor NRF2 and an epigenetic regulator, MDIG, contribute to the arsenic-induced generation of cancer stem-like cells (CSCs) as determined by applying CRISPR-Cas9 gene editing and chromosome immunoprecipitation followed by DNA sequencing (ChIP-seq).
|
Keywords | Arsenic
NRF2
MDIG
Cancer stem cells
Carcinogenesis
|
Published Date | 2021-04-03
|
Publication Title |
Seminars in Cancer Biology
|
Publisher | Elsevier
|
ISSN | 1044579X
|
Content Type |
Journal Article
|
language |
English
|
OAI-PMH Set |
岡山大学
|
Copyright Holders | © 2021 The Author(s).
|
File Version | publisher
|
PubMed ID | |
DOI | |
Related Url | isVersionOf https://doi.org/10.1016/j.semcancer.2021.03.030
|
License | http://creativecommons.org/licenses/by-nc-nd/4.0/
|
Citation | Bi Z, Zhang Q, Fu Y, Seno A, Wadgaonkar P, Qiu Y, Almutairy B, Xu L, Zhang W, Thakur C, Chen F. Cooperation between NRF2-mediated transcription and MDIG-dependent epigenetic modifications in arsenic-induced carcinogenesis and cancer stem cells. Semin Cancer Biol. 2021 Apr 3:S1044-579X(21)00080-8. doi: 10.1016/j.semcancer.2021.03.030. Epub ahead of print. PMID: 33823236.
|
Open Access (Publisher) |
OA
|
Open Archive (publisher) |
Non-OpenArchive
|