101. Propofol promotes cell apoptosis via inhibiting HOTAIR mediated mTOR pathway in cervical cancer
- Author
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Jian-hua Qian, Jun Ying, Xin-hui Zhou, Dan Zhang, Yun-xiao Zhou, Jian Zhang, and Guo-qing Wu
- Subjects
Cell Survival ,Biophysics ,Uterine Cervical Neoplasms ,Antineoplastic Agents ,Apoptosis ,Biology ,Biochemistry ,HeLa ,Mice ,Cell Line, Tumor ,Animals ,Humans ,MTT assay ,Viability assay ,Molecular Biology ,Propofol ,PI3K/AKT/mTOR pathway ,TOR Serine-Threonine Kinases ,HOTAIR ,Cell Biology ,Transfection ,biology.organism_classification ,Transplantation ,Mice, Inbred C57BL ,Cancer research ,Female ,RNA, Long Noncoding ,HeLa Cells - Abstract
Objectives Cervical cancer is one of the most common gynecologic malignant tumors. Propofol has been proposed to play a role of antitumor in various cancers. However, the functions and mechanisms of Propofol in cervical cancer is still not clear. Methods In vitro, the different concentrations of propofol were co-incubated with cervical cancer cell lines, including Hela, Caski and C-33A cells respectively. The pcDNA-HOTAIR plasmid was transfected into cells after the treatment of 10 μg/ml propofol. The cell viability and apoptosis were detected by MTT assay and TUNEL method. In vivo, propofol was injected into mice of transplantation tumor with Caski cells or with pcDNA-HOTAIR treated Caski cells. Results Propofol significantly decreased the cell viability and increased the cell apoptosis in Hela, Caski and C-33A cells, while HOTAIR overexpression promoted cell viability and inhibits cell apoptosis. mTOR/p70S6K protein expression levels were also markedly reduced by propofol but the effects were reversed with pcDNA-HOTAIR. In vivo, propofol inhibited the tumor size but had no inhibition effect in HOTAIR overexpression group. Conclusion Propofol inhibited tumor size, cell viability and promoted cell apoptosis via inhibiting mTOR/p70S6K pathway mediated by HOTAIR in cervical cancer.
- Published
- 2015