LncRNA-ATB Promotes the Tumorigenesis of Ovarian Cancer via Targeting miR-204-3p

Autor: Hong Yu, Ting Guo, Jun Ye, Hua Qian, Xiao-xiang Wang, Li Jiang, Chunyan Jin, Mei Lin, Donglan Yuan, Xia Liu
Rok vydání: 2020
Předmět:
Zdroj: OncoTargets and Therapy. 13:573-583
ISSN: 1178-6930
Popis: Background Ovarian cancer ranks fifth among the most prevalent cancer type in females all over the world. It is the second most frequent malignant tumor which accounts for 3% of cancer in females. Therefore, to explore the mechanism of carcinogenesis in ovarian cancer is important to develop new treatment methods. It has been previously found that lncRNA-ATB could promote the tumorigenesis of malignant tumors. However, the role of lncRNA-ATB during the progression of ovarian cancer remains unclear. Methods Gene expressions in tissues or cells were detected by using qRT-PCR. Western blot was performed to investigate the protein expressions in ovarian cancer cells. Cell apoptosis was tested by flow cytometry. Moreover, the correction between lncRNA-ATB and miR-204-3p was examined by Dual-luciferase reporter assay and RNA pulldown. Cell proliferation and invasion were detected by CCK-8, Ki-67 staining and transwell assay, respectively. Finally, xenograft mice model was established to confirm the result of in vitro experiments. Results LncRNA-ATB silencing significantly inhibited the proliferation and induced apoptosis of ovarian cancer cells. In addition, luciferase activity suggested that lncRNA-ATB negatively regulated miR-204-3p in ovarian cancer. Besides, Nidogen 1 (NID1) was the direct target of miR-204-3p. Overexpression of NID1 could notably reverse the inhibitory effect of lncRNA-ATB knockdown on the progression of ovarian cancer. Finally, lncRNA-ATB silencing notably attenuated the severity of ovarian cancer in vivo. Conclusion Downregulation of lncRNA-ATB significantly inhibited the tumorigenesis of ovarian cancer in vitro and in vivo, which may serve as a potential novel target for the treatment of ovarian cancer.
Databáze: OpenAIRE
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