Results
| PMID | 27694140 |
| Gene Name | SRA1 |
| Condition | Endometriosis |
| Association |
Associated |
| Sex | Female |
| Associated genes | ESR1, ESR2 |
| Other associated phenotypes |
Endometriosis |
|
Reprod Sci. 2017 Jun;24(6):836-843. doi: 10.1177/1933719116670036. Epub 2016 Sep Lin, Kaiqing| Zhan, Hong| Ma, Junyan| Xu, Kaihong| Wu, Ruijin| Zhou, Caiyun| Lin, Jun 1 Department of Gynaecology, Women's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, People's Republic of China.| 1 Department of Gynaecology, Women's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, People's Estradiol and its nuclear receptors, estrogen receptor (ER) alpha and ER-beta, have important functions in endometriosis, and the transcriptional activity of these receptors is modulated by coactivators and corepressors. The steroid receptor RNA activator 1 (SRA1) produces SRA long noncoding RNA (lncRNA) and SRA protein (SRAP), which regulate ER expression at the RNA and protein levels in some hormone-dependent tumors via an alternative splicing event. However, only a few are reported on their expressions in endometriosis. Here, we observed that low expression levels of SRA lncRNA and ER-alpha but relatively high expression levels of SRAP and ER-beta were detected in ovarian endometriotic tissues versus normal endometrial tissues. Steroid receptor RNA activator 1-small interfering RNA treatment significantly increased ER-alpha levels but reduced ER-beta levels in endometriotic stromal cells (ESCs). Furthermore, the treatment can also attenuate the proliferation and promote early apoptosis in these cells. Our results indicate that the regulation of ER via SRA in ovarian endometriosis may play a significant role in the growth of ESCs. Mesh Terms: Adult| Carrier Proteins/*genetics/metabolism| Cell Proliferation| Endometriosis/*genetics/metabolism/pathology| Female| Gene Expression Regulation| Gene Silencing| Humans| Ovarian Diseases/*genetics/metabolism/pathology| RNA, Small Interfering| |
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