In present study, we found propofol markedly decreased the HOTAIR expression of cervical cancer cells in a dose-dependent manner. In vitro experiments, we found HOTAIR overexpression promoted cervical carcinoma cells growth and inhibited cell apoptosis after the treatment of propofol.
|Cell lines||Caski cells|
|Preparation method||1 × 10^4 cells/well HeLa, CaSki and C33A cells were plated incubated in 96-well culture plates at 37℃ for 24 h, and then co-cultured with different concentrations (0 μg/ml, 1 μg/ml, 5 μg/ml and 10 μg/ml) of propofol for another 48 h.|
|Incubation time||48 h|
|Animal models||C57BL/6 mice|
|Body Surface Area (m2)||0.007||0.025||0.15||0.05||0.02||0.5|
|Animal A (mg/kg) = Animal B (mg/kg) multiplied by||Animal B Km|
|Animal A Km|
For example, to modify the dose of Compound A used for a mouse (20 mg/kg) to a dose based on the BSA for a rat, multiply 20 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for Compound A of 10 mg/kg.
|Solubility||DMSO ≥ 30 mg/mL|
Propofol promotes cell apoptosis via inhibiting HOTAIR mediated mTOR pathway in cervical cancer.
Zhang D, et al. Biochem Biophys Res Commun. 2015 Dec 25;468(4):561-7. PMID: 26523512.
Down-regulation of microRNA-21 is involved in the propofol-induced neurotoxicity observed in human stem cell-derived neurons.
Twaroski DM, et al. Anesthesiology. 2014 Oct;121(4):786-800. PMID: 24950164.
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