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. 2013 Aug 15;6(9):1799-805.
eCollection 2013.

Growth inhibitory effect of Cucurbitacin E on breast cancer cells

Tian Lan  1 , Linling Wang, Qian Xu, Weiguo Liu, Hongchuan Jin, Weimin Mao, Xian Wang, Xiaojia Wang
Affiliations

Growth inhibitory effect of Cucurbitacin E on breast cancer cells

Tian Lan et al. Int J Clin Exp Pathol. .

Abstract

Objective: Due its inhibitory effects on chemical carcinogenesis and inflammation, Cucurbitacins have been proposed as an effective agent for the prevention or treatment of human cancers. In this study, we aimed to explore the effect of Cucurbitacin E (CuE) on human breast cancer cells.

Methods: The inhibitory effect of CuE on proliferation of Bcap37 and MDA-MB-231 cells was assessed by MTT assay. The cell cycle distribution and cell apoptosis were determined by flow cytometry (FCM). The expression of pro-caspase 3, cleaved caspase 3, p21, p27 and the phosphorylation of signaling proteins was detected by Western Blotting.

Results: CuE inhibited the growth of human breast cancer cells in a dose and time-dependent manner. FCM analysis showed that CuE induced G2/M phase arrest and cell apoptosis. CuE treatment promoted the cleavage of caspase 3 and upregulated p21 and p27. In addition, the phosphorylation of STAT3 but not ERK-1/2 was abrogated upon CuE treatment. Interestingly, losedose CuE significantly enhanced the growth inhibition induced by cisplatin. Conclusions Cucurbitacin E (CuE) could inhibit the growth of human breast cancer cells in vitro. CuE induced both apoptosis and cell cycle arrest probably through the inhibition of STAT3 function. Lose-dose CuE significantly enhanced the growth inhibitory effect of cisplatin on breast cancer cells, further indicating the potential clinical values of CuE for the prevention or treatment of human breast cancer.

Keywords: Cucurbitacin E; apoptosis; breast cancer.

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Figures

Figure 1
Figure 1
CuE inhibited the growth of breast cancer cells. After the incubation with various concentrations of CuE for different times, the viability of MB-231 (A) and Bcap37 (B) cells was determined by MTT assay.
Figure 2
Figure 2
CuE induced the apoptosis of breast cancer cells. After the incubation with various concentrations of CuE for different times, the apoptosis of MB-231 (A) and Bcap37 (B) cells stained with FITC-Annexin VI and PI was determined by flowcytometry.
Figure 3
Figure 3
CuE induced cell cycle arrest in breast cancer cells. After the incubation with various concentrations of CuE for different times, the cell cycle distribution of MB-231 (A) and Bcap37 (B) cells stained with PI was determined by flowcytometry.
Figure 4
Figure 4
Effect of CuE on the expression of cell cycle regulators and signaling proteins. A: The expression of caspase-3, p21 and p27 in Bcap37 and MB-231 cells were explored by western blotting analysis. B: The phosphorylation of STAT3 and ERK (ERK-1/2) were explored by western blotting analysis.
Figure 5
Figure 5
CuE enhanced growth inhibitory effect of cisplatin. The effect of low-dose (1 μM) and high-dose (10 μM) CuE on cisplatin-induced growth inhibition in MB-231 (A) and Bcap-37 (B) cells were determined by MTT assay.
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