Long Noncoding RNA Upregulates Survivin and Facilitates Gallbladder Cancer Progression by Sponging microRNA-335.
作者信息
Yang Facai, Tang Zhaohui, Duan Anqi, Yi Bin, Shen Ningjia, Bo Zhiyuan, Yin Lei, Zhu Bin, Qiu Yinghe, Li Jingdong
机构信息
Department of General Surgery, Affiliated Hospital of North Sichuan Medical College, Nanchong 637000, People's Republic of China.
Department of General Surgery, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, People's Republic of China.
出版信息
Onco Targets Ther. 2020 Mar 20;13:2357-2367. doi: 10.2147/OTT.S236350. eCollection 2020.
BACKGROUND
Gallbladder cancer (GBC) is the most common cancer of the biliary tract, but molecularly targeted therapies are not available for GBC. Loss of microRNA (miR)-335 expression may be a useful predictor of clinical outcomes and the reversal of its loss of expression may be a useful treatment strategy for GBC. In this study, we investigated whether a long noncoding RNA, nuclear paraspeckle assembly transcript 1 () sponges in GBC cells.
MATERIALS AND METHODS
Quantitative reverse transcription-polymerase chain reaction (qRT-PCR), Western blotting, and immunohistochemistry were used to determine the expression of ; survivin; and in GBC cell lines (GBC-SD and SGC-996) and tissue samples from patients (n = 25). Cell Counting Kit-8, colony-formation, and Transwell migration and invasion assays were performed to measure cell proliferation, migration, and invasion. Bioinformatic analysis and dual-luciferase reporter assays were utilized to analyze correlativity.
RESULTS
overexpression resulted in inhibition of GBC cell proliferation and invasion. In addition, knockdown of resulted in downregulation of survivin expression. As competitively "sponges" knockdown resulted in inhibited GBC cell proliferation and invasion in vitro and GBC tumor growth in vivo. Furthermore, was found to be upregulated in GBC samples, and its expression was inversely correlated with levels, but positively correlated with survivin levels.
CONCLUSION
These findings indicate that promotes survivin expression by functioning as a competitive endogenous RNA for in GBC cells; thus, we have identified a potential biomarker and target for GBC diagnosis and therapy.
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