2. Academic Validation
  3. E2F1-regulated long non-coding RNA RAD51-AS1 promotes cell cycle progression, inhibits apoptosis and predicts poor prognosis in epithelial ovarian cancer

E2F1-regulated long non-coding RNA RAD51-AS1 promotes cell cycle progression, inhibits apoptosis and predicts poor prognosis in epithelial ovarian cancer

  • Sci Rep. 2017 Jun 30;7(1):4469. doi: 10.1038/s41598-017-04736-z.
Xiaodan Zhang 1 2 3,  Guoping Liu 4,  Junjun Qiu 1 2 3,  Ning Zhang 1 2 3,  Jingxin Ding 1 2 3,  Keqin Hua 5 6 7
Affiliations

Affiliations

  • 1 Department of Gynecology, Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China.
  • 2 Shanghai Medical College, Fudan University, Shanghai, China.
  • 3 Shanghai Key Laboratory of Female Reproductive Endocrine-Related Diseases, Fudan University, Shanghai, China.
  • 4 Institutes of Brain Science and State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, China.
  • 5 Department of Gynecology, Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China. keqinhua001@gmail.com.
  • 6 Shanghai Medical College, Fudan University, Shanghai, China. keqinhua001@gmail.com.
  • 7 Shanghai Key Laboratory of Female Reproductive Endocrine-Related Diseases, Fudan University, Shanghai, China. keqinhua001@gmail.com.
PMID: 28667302 DOI: 10.1038/s41598-017-04736-z
Abstract

Long non-coding RNA RAD51 antisense RNA 1 (RAD51-AS1, also known as TODRA) has been shown to be down-regulated by E2F1, a key cell cycle and Apoptosis regulator, in breast Cancer. Little is known regarding the role of RAD51-AS1 in disease. Here, we investigate the role of RAD51-AS1 in epithelial ovarian Cancer (EOC). Using luciferase reporter and chromatin immunoprecipitation experiments, we verified RAD51-AS1 as a target of E2F1 under negative regulation in EOC. We then examined RAD51-AS1 expression in EOC samples using in situ hybridization (ISH). RAD51-AS1 was localized to the nucleus and found to be a critical marker for clinical features that significantly correlated with poor survival in EOC patients. RAD51-AS1 was also an independent prognostic factor for EOC. Overexpression of RAD51-AS1 promoted EOC cell proliferation, while silencing of RAD51-AS1 inhibited EOC cell proliferation, delayed cell cycle progression and promoted Apoptosis in vitro and in vivo. RAD51-AS1 may participate in carcinogenesis via regulation of p53 and p53-related genes. Our study highlights the role of RAD51-AS1 as a prognostic marker of EOC. Based on its regulation of the tumor suppressor p53, RAD51-AS1-based therapy may represent a viable therapeutic option for EOC in the near future.

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