Ming Zhou1, Hao Cheng2, Yulan Fu1, Jun Zhang1. 1. Department of Gynecological Oncology, Shaanxi Cancer Hospital Affiliated to Xi'an Jiaotong University, Xi'an, China. 2. Department of Ultrasonography, Shaanxi Cancer Hospital Affiliated to Xi'an Jiaotong University, Xi'an, China.
Abstract
BACKGROUND: Ovarian cancer is a malignant tumor with a poor prognosis, its underlying mechanism is still unclear. OBJECTIVE: In this study, long noncoding RNA DARS-AS1 was studied to identify its function in the development of ovarian cancer. METHODS: Perform functional experiments to detect the effects of DARS-AS1 on the proliferation, apoptosis, and migration of ovarian cancer cells A2780. The luciferase report, immunoprecipitation (IP) experiment, and ubiquitination level determination verify that RBX1 ubiquitination and mediate the degradation of tumor suppressor gene TP53. RESULTS: Knockdown of DARS-AS1 can inhibit cell proliferation, migration, and apoptosis, and the application of miR-194-5p inhibitors can prevent this process. Luciferase and IP experiments showed that DARS-AS1 regulates the expression of RBX1 by binding to miR-194-5p, and RBX1 mediates its degradation through ubiquitination of TP53.
BACKGROUND: Ovarian cancer is a malignant tumor with a poor prognosis, its underlying mechanism is still unclear. OBJECTIVE: In this study, long noncoding RNA DARS-AS1 was studied to identify its function in the development of ovarian cancer. METHODS: Perform functional experiments to detect the effects of DARS-AS1 on the proliferation, apoptosis, and migration of ovarian cancer cells A2780. The luciferase report, immunoprecipitation (IP) experiment, and ubiquitination level determination verify that RBX1 ubiquitination and mediate the degradation of tumor suppressor gene TP53. RESULTS: Knockdown of DARS-AS1 can inhibit cell proliferation, migration, and apoptosis, and the application of miR-194-5p inhibitors can prevent this process. Luciferase and IP experiments showed that DARS-AS1 regulates the expression of RBX1 by binding to miR-194-5p, and RBX1 mediates its degradation through ubiquitination of TP53.