Bisphenol A modulates proliferation, apoptosis, and wound healing process of normal prostate cells: Involvement of G2/M-phase cell cycle arrest, MAPK signaling, and transcription factor-mediated MMP regulation
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Song, J.-H. | - |
dc.contributor.author | Hwang, B. | - |
dc.contributor.author | Kim, S.-B. | - |
dc.contributor.author | Choi, Y.H. | - |
dc.contributor.author | Kim, W.-J. | - |
dc.contributor.author | Moon, S.-K. | - |
dc.date.accessioned | 2023-10-24T05:40:54Z | - |
dc.date.available | 2023-10-24T05:40:54Z | - |
dc.date.issued | 2023-01 | - |
dc.identifier.issn | 0147-6513 | - |
dc.identifier.issn | 1090-2414 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/68264 | - |
dc.description.abstract | Bisphenol A (BPA) is commonly used to produce epoxy resins and polycarbonate plastics. BPA is an endocrine-disrupting chemical that is leaked from the polymer and absorbed into the body to disrupt the endocrine system. Although BPA may cause cytotoxicity in the prostate, a hormone-dependent reproductive organ, its underlying mechanism has not yet been elucidated. Here, we investigated the effects of BPA on cell proliferation, apoptosis, and the wound healing process using prostate epithelial cells (RWPE-1) and stromal cells (WPMY-1). Observations revealed that BPA induced G2/M cell cycle arrest in both cell types through the ATM−CHK1/CHK2–CDC25c−CDC2 signaling pathway, and the IC50 values were estimated to be 150 μM. Furthermore, BPA was found to induce caspase-dependent apoptosis through initiator (caspase-8 and −9) and executioner (caspase-3 and −7) caspase cascades. In addition, BPA interfered with the wound healing process through inhibition of MMP-2 and − 9 expression, accompanied by reductions in the binding activities of AP-1 as well as NF-κB motifs. Phosphorylation of MAPKs was associated with the BPA-mediated toxicity of prostate cells. These results suggest that BPA exhibits prostate toxicity by inhibiting cell proliferation, inducing apoptosis, and interfering with the wound healing process. Our study provided new insights into the precise molecular mechanisms of BPA-induced toxicity in human prostate cells. © 2022 The Authors | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | Academic Press | - |
dc.title | Bisphenol A modulates proliferation, apoptosis, and wound healing process of normal prostate cells: Involvement of G2/M-phase cell cycle arrest, MAPK signaling, and transcription factor-mediated MMP regulation | - |
dc.type | Article | - |
dc.identifier.doi | 10.1016/j.ecoenv.2022.114358 | - |
dc.identifier.bibliographicCitation | Ecotoxicology and Environmental Safety, v.249 | - |
dc.description.isOpenAccess | Y | - |
dc.identifier.wosid | 000976007700001 | - |
dc.identifier.scopusid | 2-s2.0-85143596234 | - |
dc.citation.title | Ecotoxicology and Environmental Safety | - |
dc.citation.volume | 249 | - |
dc.type.docType | Article | - |
dc.publisher.location | 미국 | - |
dc.subject.keywordAuthor | Bisphenol A | - |
dc.subject.keywordAuthor | Cell cycle | - |
dc.subject.keywordAuthor | MMP-9 | - |
dc.subject.keywordAuthor | Prostate cells | - |
dc.subject.keywordAuthor | Wound healing process | - |
dc.subject.keywordPlus | THULIUM LASER | - |
dc.subject.keywordPlus | MIGRATION | - |
dc.subject.keywordPlus | RATS | - |
dc.relation.journalResearchArea | Environmental Sciences & Ecology | - |
dc.relation.journalResearchArea | Toxicology | - |
dc.relation.journalWebOfScienceCategory | Environmental Sciences | - |
dc.relation.journalWebOfScienceCategory | Toxicology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
84, Heukseok-ro, Dongjak-gu, Seoul, Republic of Korea (06974)02-820-6194
COPYRIGHT 2019 Chung-Ang University All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.