Affiliations: [a] Department of Imaging, Yantai Yuhuangding Hospital, Yantai, Shandong, China | [b] Department of Anesthesiology, Yantai Yuhuangding Hospital, Yantai, Shandong, China | [c] Department of Clinical Laboratory, The Affiliated Hospital of Weifang Medical College, Weifang, Shandong, China
Correspondence:
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Corresponding author: Liping Wang, Department of Imaging, Yantai Yuhuangding Hospital, Yantai, Shandong, China. E-mail: [email protected].
Note: [1] Benxia Yu and Wei Gao were equal to the work.
Abstract: BACKGROUND AND OBJECTIVE:Propofol, an intravenous anesthetic agent, has been found to inhibit growth of breast cancer cells. However, the mechanisms underlying the antitumor are not known. A recent report has found that propofol could significantly downregulate miR-24 expression in the human malignant cancers. In breast cancer cells, overexpression of miR-24 promotes cell proliferation and inhibits cell apoptosis by downregulation of p27. The miR-24 has been reported to be overexpressed in breast cancer and breast cancer cell lines. In the present study, we hypothesized that propofol induces apoptosis of breast cancer cells by miR-24/p27 signal pathway. METHODS: Breast cancer MDA-MB-435 cells were exposed to propofol (10 μM) for 6 hr and cell death was assessed using TUNEL staining, Flow cytometry and cleaved caspase-3 expression. microRNA-24 (miR-24) expression was assessed using quantitative reverse transcription polymerase chain reaction (qRT-PCR). miR-24 was overexpressed using a miR-24 mimic. P27 was knocked down using a small interfering RNA. p27 and cleaved caspase-3 expression was assessed by Western blot. RESULTS: MDA-MB-435 exposed to propofol showed a significant increase in apoptotic cells, followed by the downregulation of miR-24, upregulation of p27 expression and cleaved caspase-3 expression. Targeting p27 inhibits propofol-induced cell apoptosis; miR-24 overexpression decreased propofol-induced cell apoptosis, cleaved caspase-3 and p27 expression. CONCLUSIONS: Propofol inducescell death in MDA-MB-435 cells via inactivation of miR-24/p27 signal pathway.
