Abstract
Propofol is an intravenous sedative hypnotic agent of which the growth-inhibitory effect has been reported on various cancers. However, the roles of propofol in endometrial cancer (EC) remain unclear. This study aimed to explore the effects of propofol on EC in vitro and in vivo. Different concentrations of propofol were used to treat Ishikawa cells. Colony number, cell viability, cell cycle, apoptosis, migration, and invasion were analyzed by colony formation, MTT, flow cytometry, and Transwell assays. In addition, the pcDNA3.1-Sox4 and Sox4 siRNA plasmids were transfected into Ishikawa cells to explore the relationship between propofol and Sox4 in EC cell proliferation. Tumor weight in vivo was measured by xenograft tumor model assay. Protein levels of cell cycle-related factors, apoptosis-related factors, matrix metalloproteinases 9 (MMP9), matrix metalloproteinases 2 (MMP2) and Wnt/β-catenin pathway were examined by western blot. Results showed that propofol significantly decreased colony numbers, inhibited cell viability, migration, and invasion but promoted apoptosis in a dose-dependent manner in Ishikawa cells. Moreover, propofol reduced the expression of Sox4 in a dose-dependent manner. Additionally, propofol significantly suppressed the proportions of Ki67+ cells, but Sox4 overexpression reversed the results. Furthermore, in vivo assay results showed that propofol inhibited tumor growth; however, the inhibitory effect was abolished by Sox4 overexpression. Moreover, propofol inhibited Sox4 expression via inactivation of Wnt/β-catenin signal pathway. Our study demonstrated that propofol inhibited cell proliferation, migration, and invasion but promoted apoptosis by regulation of Sox4 in EC cells. These findings might indicate a novel treatment strategy for EC.
Highlights
Endometrial cancer (EC) is one of the most common malignancies of the female reproductive system [1,2]
The inhibitory effects of propofol on Ki67+ cells were significantly abolished by Sex-determining region Y-box 4 (Sox4) overexpression (Po0.05 or Po0.01, Figure 4D). These results suggested that Sox4 overexpression could alleviate the inhibitory effect of propofol on cell proliferation by down-regulation of Sox4 in Ishikawa cells
We found that propofol significantly decreased cell proliferation, migration, and invasion but promoted apoptosis in a dose-dependent manner in Ishikawa cells
Summary
Endometrial cancer (EC) is one of the most common malignancies of the female reproductive system [1,2]. More than 200,000 women suffer from EC every year, and the mortality rate is just behind ovarian cancer and cervical cancer [3]. The primary treatment for EC is surgery followed by adjuvant radiation therapy and chemotherapy [4]. These therapies have not effectively reduced the risk of EC mortality. The recurrence rates of EC are higher than 60–80% two to three years after surgery [5]. An increasing number of studies have demonstrated that anesthetics and anesthetic techniques have beneficial effects on postoperative recurrence and could improve survival rate in various cancers [6,7]. The effect of anesthetics on EC and its molecular mechanism remain unclear
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