ASB13 inhibits breast cancer metastasis through promoting SNAI2 degradation and relieving its transcriptional repression of YAP. Author Huijuan Fan, Xuxiang Wang, Wenyang Li, Minhong Shen, Yong Wei, Hanqiu Zheng, Yibin Kang Publication Year 2020 Type Journal Article Abstract Transcription factor SNAI2 plays key roles during development and has also been known to promote metastasis by inducing invasive phenotype and tumor-initiating activity of cancer cells. However, the post-translational regulation of SNAI2 is less well studied. We performed a dual-luciferase-based, genome-wide E3 ligase siRNA library screen and identified ASB13 as an E3 ubiquitin ligase that targets SNAI2 for ubiquitination and degradation. ASB13 knockout in breast cancer cells promoted cell migration and decreased F-actin polymerization, while overexpression of ASB13 suppressed lung metastasis. Furthermore, ASB13 knockout decreased YAP expression, and such regulation is dependent on an increased protein level of SNAI2, which in turn represses YAP transcription. YAP suppresses tumor progression in breast cancer, as YAP knockout increases tumorsphere formation, anchorage-independent colony formation, cell migration in vitro, and lung metastasis in vivo. Clinical data analysis reveals that ASB13 expression is positively correlated with improved overall survival in breast cancer patients. These findings establish ASB13 as a suppressor of breast cancer metastasis by promoting degradation of SNAI2 and relieving its transcriptional repression of YAP. Keywords Humans, Female, Ubiquitin-Protein Ligases, Cell Line, Tumor, RNA, Small Interfering, Cell Movement, Breast Neoplasms, Gene Expression Regulation, Neoplastic, Proteolysis, Genome-Wide Association Study, Ubiquitination, Neoplasm Metastasis, Snail Family Transcription Factors, Proto-Oncogene Proteins c-yes Journal Genes Dev Volume 34 Issue 19-20 Pages 1359-1372 Date Published 2020 Oct 01 ISSN Number 1549-5477 DOI 10.1101/gad.339796.120 Alternate Journal Genes Dev PMCID PMC7528707 PMID 32943576 PubMedPubMed CentralGoogle ScholarBibTeXEndNote X3 XML