Details

Autor(en) / Beteiligte

• Zhang, Dan
• Zhou, Xin-hui
• Zhang, Jian
• Zhou, Yun-xiao
• Ying, Jun
• Wu, Guo-qing
• Qian, Jian-hua

Titel

Propofol promotes cell apoptosis via inhibiting HOTAIR mediated mTOR pathway in cervical cancer

Ist Teil von

• Biochemical and biophysical research communications, 2015-12, Vol.468 (4), p.561-567

Ort / Verlag

United States: Elsevier Inc

Erscheinungsjahr

2015

Link zum Volltext

Quelle

MEDLINE

Beschreibungen/Notizen

• 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. 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. 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. Propofol inhibited tumor size, cell viability and promoted cell apoptosis via inhibiting mTOR/p70S6K pathway mediated by HOTAIR in cervical cancer. •Propofol inhibited cell growth and increased cell apoptosis in cervical cancer.•Propofol reduced tumor size of cervical cancer in vivo.•HOTAIR overexpression promotes cervical carcinoma cell growth via mTOR regulation.•HOTAIR was involved in the effects of propofol on cervical cancer cell growth.