Epigallocatechin-3-gallate reduces the proliferation of benign prostatic hyperplasia cells via regulation of focal adhesions

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dc.contributor.authorTepedelen B.E.
dc.contributor.authorSoya E.
dc.contributor.authorKorkmaz M.
dc.date.accessioned2024-07-22T08:10:23Z
dc.date.available2024-07-22T08:10:23Z
dc.date.issued2017
dc.description.abstractAims Benign prostatic hyperplasia (BPH) is the most common urological disease that is characterized by the excessive growth of prostatic epithelial and stromal cells. Pharmacological therapy for BPH has limited use due to the many side effects so there is a need for new agents including natural compounds such as epigallocatechin-3-gallate (EGCG). This study was undertaken to assess the role of EGCG, suppressing the formation of BPH by reducing inflammation and oxidative stress, in cytoskeleton organization and ECM interactions via focal adhesions. Main methods We performed MTT assay to investigate cell viability of BPH-1 cells, wound healing assay to examine cell migration, immunofluorescence assay for F-actin organization and paxillin distribution and finally immunoblotting to investigate focal adhesion protein levels in the presence and absence of EGCG. Key findings We found that EGCG inhibits cell proliferation at the concentration of 89.12 μM, 21.2 μM and 2.39 μM for 24, 48 and 72 h, respectively as well as inhibitory effects of EGCG on BPH-1 cell migration were observed in a wound healing assay. Furthermore, it was determined by immunofluorescence labeling that EGCG disrupts F-actin organization and reduces paxillin distribution. Additionally, EGCG decreases the activation of FAK (Focal Adhesion Kinase) and the levels of paxillin, RhoA (Ras homolog gene family, member A), Cdc42 (cell division cycle 42) and PAK1 (p21 protein-activated kinase 1) in a dose-dependent manner. Significance For the first time, by this study, we found evidence that BPH-1 cell proliferation could be inhibited with EGCG through the disruption of cytoskeleton organization and ECM interactions. Consequently, EGCG might be useful in the prevention and treatment of diseases characterized by excessive cell proliferation such as BPH. © 2017
dc.identifier.DOI-ID10.1016/j.lfs.2017.10.016
dc.identifier.issn00243205
dc.identifier.urihttp://akademikarsiv.cbu.edu.tr:4000/handle/123456789/15218
dc.language.isoEnglish
dc.publisherElsevier Inc.
dc.subjectActin Cytoskeleton
dc.subjectActins
dc.subjectAnticarcinogenic Agents
dc.subjectCatechin
dc.subjectCell Line
dc.subjectCell Movement
dc.subjectCell Proliferation
dc.subjectCell Survival
dc.subjectFocal Adhesions
dc.subjectHumans
dc.subjectMale
dc.subjectProstatic Hyperplasia
dc.subjectepigallocatechin gallate
dc.subjectF actin
dc.subjectfocal adhesion kinase
dc.subjectp21 activated kinase 1
dc.subjectpaxillin
dc.subjectprotein Cdc42
dc.subjectRhoA guanine nucleotide binding protein
dc.subjectactin
dc.subjectantineoplastic agent
dc.subjectcatechin
dc.subjectepigallocatechin gallate
dc.subjectactin filament
dc.subjectantiinflammatory activity
dc.subjectantiproliferative activity
dc.subjectArticle
dc.subjectBPH-1 cell line
dc.subjectcellular distribution
dc.subjectconcentration response
dc.subjectcontrolled study
dc.subjectextracellular matrix
dc.subjectfocal adhesion
dc.subjecthuman
dc.subjecthuman cell
dc.subjectmigration inhibition
dc.subjectprostatic hyperplasia cell line
dc.subjectwound healing assay
dc.subjectanalogs and derivatives
dc.subjectcell line
dc.subjectcell motion
dc.subjectcell proliferation
dc.subjectcell survival
dc.subjectdrug effects
dc.subjectfocal adhesion
dc.subjectmale
dc.subjectmetabolism
dc.subjectpathology
dc.subjectprostate hypertrophy
dc.titleEpigallocatechin-3-gallate reduces the proliferation of benign prostatic hyperplasia cells via regulation of focal adhesions
dc.typeArticle

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