作者: Tae Gyu Oh , Shu-Ching M. Wang , Bipul R. Acharya , Joel M. Goode , J. Dinny Graham
DOI: 10.1016/J.EBIOM.2016.02.028
关键词:
摘要: Abstract We have previously reported that RORγ expression was decreased in ER−ve breast cancer, and increased improves clinical outcomes. However, the underlying dependent mechanisms repress carcinogenesis not been elucidated. Here we report negatively regulates oncogenic TGF-β/EMT mammary stem cell (MaSC) pathways, whereas positively DNA-repair. demonstrate is: (i) basal-like subtype cancers, (ii) inversely correlated with histological grade drivers of cancer cohorts. Furthermore, integration RNA-seq ChIP-chip data reveals many genes involved TGF-β/EMT-signaling, DNA-repair MaSC pathways (including non-coding RNA, LINC00511). In accordance, pharmacological studies an agonist suppresses viability, migration, EMT transition (microsphere outgrowth) mammosphere-growth. contrast, demonstrates inverse induces TGF-β/EMT-signaling. These findings suggest modulation activity may utility cancer.