MiR‐655 suppresses epithelial‐to‐mesenchymal transition by targeting Prrx1 in triple‐negative breast cancer. Issue 5 (28th January 2016)

• Record Type: Journal Article
• Authors: Lv, Zhi‐Dong; Kong, Bin; Liu, Xiang‐Ping; Jin, Li‐Ying; Dong, Qian; Li, Fu‐Nian; Wang, Hai‐Bo
• Is Part Of: Journal of cellular and molecular medicine. Volume 20:Issue 5(2016)
• Page Start: 864
• Page End: 873
• Publication Date: 2016-01-28
• Subjects: miR‐655 -- triple‐negative breast cancer -- Prrx1 -- epithelial‐to‐mesenchymal transition; Cytology; Medicine; Molecular Biology; Cytologie -- Périodiques; Médecine -- Périodiques; Biologie moléculaire -- Périodiques; Cytology -- Periodicals; Medicine -- Periodicals; Molecular biology -- Periodicals; 611.01805
• DOI: 10.1111/jcmm.12770
• Languages: English
• ISSNs: 1582-1838

Abstract

Abstract: Triple‐negative breast cancer (TNBC) is a highly aggressive breast cancer subtype that lacks effective targeted therapies. The epithelial‐to‐mesenchymal transition (EMT) is a key contributor in the metastatic process. In this study, we found that miR‐655 was down‐regulated in TNBC, and its expression levels were associated with molecular‐based classification and lymph node metastasis in breast cancer. These findings led us to hypothesize that miR‐655 overexpression may inhibit EMT and its associated traits of TNBC. Ectopic expression of miR‐655 not only induced the up‐regulation of cytokeratin and decreased vimentin expression but also suppressed migration and invasion of mesenchymal‐like cancer cells accompanied by a morphological shift towards the epithelial phenotype. In addition, we found that miR‐655 was negatively correlated with Prrx1 in cell lines and clinical samples. Overexpression of miR‐655 significantly suppressed Prrx1, as demonstrated by Prrx1 3′‐untranslated region luciferase report assay. Our study demonstrated that miR‐655 inhibits the acquisition of the EMT phenotype in TNBC by down‐regulating Prrx1, thereby inhibiting cell migration and invasion during cancer progression.