دورية أكاديمية

miR-1202 regulates BPH-1 cell proliferation, apoptosis, and epithelial-to-mesenchymal transition through targeting HMGCL.

التفاصيل البيبلوغرافية
العنوان: miR-1202 regulates BPH-1 cell proliferation, apoptosis, and epithelial-to-mesenchymal transition through targeting HMGCL.
المؤلفون: Wang Z, Yin X, Yang P, Gong B, Liu H
المصدر: Acta biochimica et biophysica Sinica [Acta Biochim Biophys Sin (Shanghai)] 2024 May 25; Vol. 56 (5), pp. 675-687.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: China Science Publishing & Media Ltd Country of Publication: China NLM ID: 101206716 Publication Model: Print Cited Medium: Internet ISSN: 1745-7270 (Electronic) Linking ISSN: 16729145 NLM ISO Abbreviation: Acta Biochim Biophys Sin (Shanghai) Subsets: MEDLINE
أسماء مطبوعة: Publication: 2022- : Shanghai : China Science Publishing & Media Ltd.
Original Publication: Shanghai : Shanghai Scientific and Technical Publishers, 2004-
مواضيع طبية MeSH: Apoptosis*/genetics , Apoptosis*/drug effects , Cell Proliferation*/genetics , Cell Proliferation*/drug effects , Epithelial-Mesenchymal Transition*/genetics , Epithelial-Mesenchymal Transition*/drug effects , MicroRNAs*/genetics , MicroRNAs*/metabolism , Prostatic Hyperplasia*/pathology , Prostatic Hyperplasia*/metabolism , Prostatic Hyperplasia*/genetics, Animals ; Humans ; Male ; Rats ; Cell Line ; Transforming Growth Factor beta/metabolism ; Wnt Signaling Pathway/genetics ; Wnt Signaling Pathway/drug effects
مستخلص: Benign prostatic hyperplasia (BPH) is the expansion of the prostate gland that results in urinary symptoms. Both the epithelial-to-mesenchymal transition (EMT) and the Wnt signaling pathway are associated with BPH pathology. In this study, we find that miR-1202 is increased in BPH samples. Overexpression of miR-1202 in TGF-β-treated BPH-1 cells enhances cell survival and DNA synthesis and inhibits cell apoptosis, whereas miR-1202 inhibition partially abolishes the effects of TGF-β on BPH-1 cells. miR-1202 overexpression reduces E-cadherin level but elevates vimentin, N-cadherin, and snail levels, whereas miR-1202 inhibition partially attenuates the effects of TGF-β on EMT markers. Regarding the Wnt/β-catenin pathway, miR-1202 overexpression significantly enhances, whereas miR-1202 inhibition partially decreases, the promotive effects of TGF-β on Wnt1, c-Myc, and cyclin D1 proteins. 3-Hydroxy-3-methylglutaryl-CoA lyase (HMGCL) is a direct downstream target of miR-1202, and miR-1202 inhibits HMGCL expression through binding to its 3'UTR. Overexpression of HMGCL significantly reduces the effect of miR-1202 overexpression on the phenotypes of BPH-1 cells by inhibiting cell survival and promoting apoptosis. Similarly, HMGCL overexpression has the opposite effects on EMT markers and the Wnt/β-catenin signaling, and markedly alleviates the effects of miR-1202 overexpression. Finally, in the BPH rat model, Ki67 and vimentin levels are elevated, but E-cadherin and HMGCL levels are reduced. In conclusion, miR-1202 is upregulated in benign prostatic hyperplasia; miR-1202 enhances epithelial cell proliferation, suppresses cell apoptosis, and promotes EMT by targeting HMGCL. The Wnt/β-catenin pathway may participate in the miR-1202/HMGCL axis-mediated regulation of BPH-1 cell phenotypes.
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فهرسة مساهمة: Keywords: 3-hydroxy-3-methylglutaryl-CoA lyase (HMGCL); Wnt/β-catenin pathway; benign prostate hyperplasia (BPH); epithelial-to-mesenchymal transition (EMT); miR-1202
المشرفين على المادة: 0 (MicroRNAs)
0 (Transforming Growth Factor beta)
EC 4.1.3.4 (3-hydroxy-3-methylglutaryl-coenzyme A lyase)
تواريخ الأحداث: Date Created: 20240329 Date Completed: 20240530 Latest Revision: 20240616
رمز التحديث: 20240616
مُعرف محوري في PubMed: PMC11177111
DOI: 10.3724/abbs.2024001
PMID: 38551020
قاعدة البيانات: MEDLINE
الوصف
تدمد:1745-7270
DOI:10.3724/abbs.2024001