LncRNA DANCR upregulates PI3K/AKT signaling through activating serine phosphorylation of RXRA. Issue 12 (December 2018)

• Record Type: Journal Article
• Authors: Tang, Jianming; Zhong, Guangsheng; Zhang, Haibo; Yu, Bo; Wei, Fangqiang; Luo, Liming; kang, Yao; Wu, Jianhui; Jiang, Jiaxiang; Li, Yucheng; Wu, Shuqiang; Jia, Yongshi; Liang, Xiaodong; Bi, Aihong
• Is Part Of: Cell death and disease. Volume 9:Issue 12(2018)
• Page Start: 1
• Page End: 12
• Publication Date: 2018-12
• Subjects: Cell death -- Periodicals; Apoptosis -- Periodicals; 571.936
• DOI: 10.1038/s41419-018-1220-7
• Languages: English
• ISSNs: 2041-4889

Abstract

Abstact Conventional therapies and novel molecular targeted therapies against breast cancer have gained great advances over the past two decades. However, poor prognosis and low survival rate are far from expectation for improvement, particularly in patients with triple negative breast cancer (TNBC). Here, we found that lncRNADANCR was significantly overregulated in TNBC tissues and cell lines compared with normal breast tissues or other type of breast cancer. Knockdown ofDANCR suppressed TNBC proliferation both in vitro and in vivo. Further study of underlying mechanisms demonstrated thatDANCR bound with RXRA and increased its serine 49/78 phosphorylation via GSK3β, resulting in activating PIK3CA transcription, and subsequently enhanced PI3K/AKT signaling and TNBC tumorigenesis. Taken together, Our findings identifiedDANCR as an pro-oncogene and uncoverd a new working pattern of lncRNA to mediate TNBC tumorigenesis, which may be a potential therapeutic target for improving treatment of TNBC.