| الوصف: |
Ying-Ji Fang,1,* Ping Jiang,2,* Hui Zhai,1 Jing-Sen Dong1 1Department of Gynecology, Jinan Maternal and Child Care Hospital, Jinan, Shandong, People’s Republic of China; 2Department of Obstetrics, Yantai Mountain Hospital, Yantai, Shandong, People’s Republic of China*These authors contributed equally to this workCorrespondence: Ping Jiang Department of Obstetrics, Yantai Mountain Hospital, Yantai, Shandong, People’s Republic of ChinaEmail jiangcong7587@126.comBackground: Early detection and diagnosis of ovarian cancer (OC) is complicated due to the concealment of the ovarian anatomical position and the lack of clinical manifestations and specific indicators of early OC. Therefore, it is urgent to study the pathogenesis of OC, especially the molecular mechanism.Results: LncRNA GAS8-AS1 was decreased in OC tissues and cell lines, and high expression of GAS8-AS1 indicated a higher 5-year survival rate of OC patients. Overexpression of GAS8-AS1 suppressed growth of OC cells, while deletion of GAS8-AS1 promoted the progression of OC cells. Further data indicated GAS8-AS1 activated autophagy in OC cells. Functional experiments showed that 3-MA removed the inhibitory effect of GAS8-AS1 in OC cells. On the contrary, Rapamycin reversed the promoting effect of GAS8-AS1 in OC cells. Furthermore, GAS8-AS1 bound with Beclin1 and promoted its expression, and silencing of Beclin1 reversed the inhibitory role of GAS8-AS1 in OC progression. In vivo tumorigenesis assay showed GAS8-AS1 suppressed OC progression and activated Beclin1 mediated autophagy.Conclusion: Our study suggested GAS8-AS1 inhibited OC progression by activating autophagy via binding with Beclin1, and GAS8-AS1 might be a potential therapeutic target for OC clinical treatment.Keywords: ovarian cancer, GAS8-AS1, autophagy, Beclin1, tumor progression |
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