Silencing of Prrx1b suppresses cellular proliferation, migration, invasion and epithelial–mesenchymal transition in triple‐negative breast cancer. Issue 9 (29th March 2016)

• Record Type: Journal Article
• Authors: Lv, Zhi‐Dong; Yang, Zhao‐Chuan; Liu, Xiang‐Ping; Jin, Li‐Ying; Dong, Qian; Qu, Hui‐Li; Li, Fu‐Nian; Kong, Bin; Sun, Jiao; Zhao, Jiao‐Jiao; Wang, Hai‐Bo
• Is Part Of: Journal of cellular and molecular medicine. Volume 20:Issue 9(2016)
• Page Start: 1640
• Page End: 1650
• Publication Date: 2016-03-29
• Subjects: triple‐negative breast cancer -- paired‐related homeobox 1b -- epithelial–mesenchymal transition -- proliferation -- invasion; Cytology; Medicine; Molecular Biology; Cytologie -- Périodiques; Médecine -- Périodiques; Biologie moléculaire -- Périodiques; Cytology -- Periodicals; Medicine -- Periodicals; Molecular biology -- Periodicals; 611.01805
• DOI: 10.1111/jcmm.12856
• Languages: English
• ISSNs: 1582-1838

Abstract

Abstract: Triple‐negative breast cancer (TNBC) is a highly aggressive tumour subtype associated with poor prognosis. The mechanisms involved in TNBC progression remains largely unknown. To date, there are no effective therapeutic targets for this tumour subtype. Paired‐related homeobox 1b (Prrx1b), one of major isoforms of Prrx1, has been identified as a new epithelial–mesenchymal transition (EMT) inducer. However, the function of Prrx1b in TNBC has not been elucidated. In this study, we found that Prrx1b was significantly up‐regulated in TNBC and associated with tumour size and vascular invasion of breast cancer. Silencing of Prrx1b suppressed the proliferation, migration and invasion of basal‐like cancer cells. Moreover, silencing of Prrx1b prevented Wnt/β‐catenin signaling pathway and induced the mesenchymal‐epithelial transition (MET). Taken together, our data indicated that Prrx1b may be an important regulator of EMT in TNBC cells and a new therapeutic target for interventions against TNBC invasion and metastasis.