دورية أكاديمية
أعرض في EDS

OVOL1 inhibits breast cancer cell invasion by enhancing the degradation of TGF-β type I receptor.

التفاصيل البيبلوغرافية
العنوان: OVOL1 inhibits breast cancer cell invasion by enhancing the degradation of TGF-β type I receptor.
المؤلفون: Fan C; Department of Cell and Chemical Biology, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands.; Oncode Institute, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands., Wang Q; Department of Cell and Chemical Biology, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands., van der Zon G; Department of Cell and Chemical Biology, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands.; Oncode Institute, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands., Ren J; Department of Cell and Chemical Biology, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands., Agaser C; Department of Biomedical Data Sciences, Sequencing Analysis Support Core, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands., Slieker RC; Department of Cell and Chemical Biology, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands.; Department of Epidemiology and Data Science, Amsterdam Public Health Institute, Amsterdam Cardiovascular Sciences Institute, Amsterdam UMC, location VUmc, Amsterdam, 1081 HV, The Netherlands., Iyengar PV; Department of Cell and Chemical Biology, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands.; Oncode Institute, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands., Mei H; Department of Biomedical Data Sciences, Sequencing Analysis Support Core, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands., Ten Dijke P; Department of Cell and Chemical Biology, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands. p.ten_dijke@lumc.nl.; Oncode Institute, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands. p.ten_dijke@lumc.nl.
المصدر: Signal transduction and targeted therapy [Signal Transduct Target Ther] 2022 Apr 29; Vol. 7 (1), pp. 126. Date of Electronic Publication: 2022 Apr 29.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Nature Publishing Group Country of Publication: England NLM ID: 101676423 Publication Model: Electronic Cited Medium: Internet ISSN: 2059-3635 (Electronic) Linking ISSN: 20593635 NLM ISO Abbreviation: Signal Transduct Target Ther Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [London] : Nature Publishing Group, [2016]-
مواضيع طبية MeSH: Breast Neoplasms*/genetics , Breast Neoplasms*/pathology, DNA-Binding Proteins ; Epithelial-Mesenchymal Transition/genetics ; Female ; Humans ; Neoplasm Invasiveness/genetics ; Neoplasm Invasiveness/pathology ; Receptor, Transforming Growth Factor-beta Type I/genetics ; Transcription Factors ; Transforming Growth Factor beta/genetics
مستخلص: Ovo-like transcriptional repressor 1 (OVOL1) is a key mediator of epithelial lineage determination and mesenchymal-epithelial transition (MET). The cytokines transforming growth factor-β (TGF-β) and bone morphogenetic proteins (BMP) control the epithelial-mesenchymal plasticity (EMP) of cancer cells, but whether this occurs through interplay with OVOL1 is not known. Here, we show that OVOL1 is inversely correlated with the epithelial-mesenchymal transition (EMT) signature, and is an indicator of a favorable prognosis for breast cancer patients. OVOL1 suppresses EMT, migration, extravasation, and early metastatic events of breast cancer cells. Importantly, BMP strongly promotes the expression of OVOL1, which enhances BMP signaling in turn. This positive feedback loop is established through the inhibition of TGF-β receptor signaling by OVOL1. Mechanistically, OVOL1 interacts with and prevents the ubiquitination and degradation of SMAD family member 7 (SMAD7), which is a negative regulator of TGF-β type I receptor stability. Moreover, a small-molecule compound 6-formylindolo(3,2-b)carbazole (FICZ) was identified to activate OVOL1 expression and thereby antagonizing (at least in part) TGF-β-mediated EMT and migration in breast cancer cells. Our results uncover a novel mechanism by which OVOL1 attenuates TGF-β/SMAD signaling and maintains the epithelial identity of breast cancer cells.
(© 2022. The Author(s).)
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المشرفين على المادة: 0 (DNA-Binding Proteins)
0 (OVOL1 protein, human)
0 (Transcription Factors)
0 (Transforming Growth Factor beta)
EC 2.7.11.30 (Receptor, Transforming Growth Factor-beta Type I)
تواريخ الأحداث: Date Created: 20220428 Date Completed: 20220502 Latest Revision: 20220716
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC9050647
DOI: 10.1038/s41392-022-00944-w
PMID: 35484112
قاعدة البيانات: MEDLINE
الوصف
تدمد:2059-3635
DOI:10.1038/s41392-022-00944-w