Steroid receptor RNA activator: Biologic function and role in disease.
Steroid receptor RNA activator (SRA) is a type of long noncoding RNA (lncRNA) which coordinates the functions of various transcription factors, enhances steroid receptor-dependent gene expression, and also serves as a distinct scaffold. The novel, profound and expanded roles of SRA are emerging in critical aspects of coactivation of nuclear receptors (NRs). As a nuclear receptor coactivator, SRA can coactivate androgen receptor (AR), estrogen receptor α (ERα), ERβ, progesterone receptor (PR), glucocorticoid receptor (GR), thyroid hormone receptor and retinoic acid receptor (RAR). Although SRA is one of the least well-understood molecules, increasing studies have revealed that SRA plays a key role in both biological processes, such as myogenesis and steroidogenesis, and pathological changes, including obesity, cardiomyopathy, and tumorigenesis. Furthermore, the SRA-related signaling pathways, such as the mitogen-activated protein kinase (p38 MAPK), Notch and tumor necrosis factor α (TNFα) pathways, play critical roles in the pathogenesis of estrogen-dependent breast cancers. In addition, the most recent data demonstrates that SRA expression may serve as a new prognostic marker in patients with ER-positive breast cancer. Thus, elucidating the molecular mechanisms underlying SRA-mediated functions is important to develop proper novel strategies to target SRA in the diagnosis and treatment of human diseases.
School of Pharmacy, Hunan University of Chinese Medicine, Changsha, Hunan, China; Institute of Pharmacy and Pharmacology, University of South China, Hengyang, Hunan, China.
Chan
C
Liu
The Second Xiangya Hospital, Central South University, Changsha, China.
Hong-Tao
HT
Wu
The First Hospital of Hunan University of Chinese Medicine, Changsha, China.
Neng
N
Zhu
School of Pharmacy, Hunan University of Chinese Medicine, Changsha, Hunan, China.
Ya-Ning
YN
Shi
School of Pharmacy, Hunan University of Chinese Medicine, Changsha, Hunan, China; Institute of Pharmacy and Pharmacology, University of South China, Hengyang, Hunan, China.
Zheng
Z
Liu
School of Pharmacy, Hunan University of Chinese Medicine, Changsha, Hunan, China; Institute of Pharmacy and Pharmacology, University of South China, Hengyang, Hunan, China.
Bao-Xue
BX
Ao
School of Pharmacy, Hunan University of Chinese Medicine, Changsha, Hunan, China.
Duan-Fang
DF
Liao
School of Pharmacy, Hunan University of Chinese Medicine, Changsha, Hunan, China; Department of Biochemistry & Molecular Biology, Libin Cardiovascular Institute of Alberta, Cumming School of Medicine, University of Calgary, Calgary, Alberta T2N 4N1, Canada.
Xi-Long
XL
Zheng
School of Pharmacy, Hunan University of Chinese Medicine, Changsha, Hunan, China. Electronic address: lqin1011@126.com.
Li
L
Qin
D002318:Cardiovascular Diseases / Q000378:metabolism*; D005260:Female; D006801:Humans; D009369:Neoplasms / Q000378:metabolism*; D009765:Obesity / Q000378:metabolism*; D011085:Polycystic Ovary Syndrome / Q000378:metabolism*; D062085:RNA, Long Noncoding / Q000737:chemistry / Q000235:genetics / Q000378:metabolism*
D062085:RNA, Long Noncoding; C405423:steroid receptor RNA activator
Long noncoding RNAs; Nuclear receptor; SRA; Transcriptional coactivator