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Cucurbitacin E induces cell cycle G2/M phase arrest and apoptosis in triple negative breast cancer.

Kong Y, Chen J, Zhou Z, Xia H, Qiu MH, Chen C - PLoS ONE (2014)

Bottom Line: In this study, we compared the effects of 12 phytochemical drugs on four cancer cell lines, and noticed that Cucurbitacin E (CuE) significantly inhibited TNBC cell growth by inducing cell cycle G2/M phase arrest and apoptosis.CuE reduced expression of Cyclin D1, Survivin, XIAP, Bcl2, and Mcl-1 in MDA-MB-468 and SW527, and within MDA-MB-468, CuE significantly increased activation of JNK and inhibited activation of AKT and ERK.Collectively, these results suggest that CuE may be a viable compound for developing novel TNBC therapeutics.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, China; Kunming College of Life Science, University of Chinese Academy of Sciences, Kunming, Yunnan, China.

ABSTRACT
Triple negative breast cancer (TNBC) is a highly aggressive form of breast cancer resistant to many common treatments. In this study, we compared the effects of 12 phytochemical drugs on four cancer cell lines, and noticed that Cucurbitacin E (CuE) significantly inhibited TNBC cell growth by inducing cell cycle G2/M phase arrest and apoptosis. CuE reduced expression of Cyclin D1, Survivin, XIAP, Bcl2, and Mcl-1 in MDA-MB-468 and SW527, and within MDA-MB-468, CuE significantly increased activation of JNK and inhibited activation of AKT and ERK. Collectively, these results suggest that CuE may be a viable compound for developing novel TNBC therapeutics.

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CuE induces cell cycle G2/M arrest in MDA-MB-468 and SW527 TNBC cell lines.A. MDA-MB-468 and SW527 cells were treated with CuE (0–50–100–200 nM) for 24 h. Cells were stained with PI and analyzed by flow cytometry. The cell cycle graph was analyzed by FlowJo software (version 7.6). B. CuE significantly increased the percentage of G2/M phase MDA-MB-468 cells compared to DMSO. ** p<0.01, *** p<0.001, student t-test. C. CuE significantly increased the percentage of G2/M phase SW527 cells compared to DMSO. ** p<0.01, *** p<0.001, student t-test.
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pone-0103760-g003: CuE induces cell cycle G2/M arrest in MDA-MB-468 and SW527 TNBC cell lines.A. MDA-MB-468 and SW527 cells were treated with CuE (0–50–100–200 nM) for 24 h. Cells were stained with PI and analyzed by flow cytometry. The cell cycle graph was analyzed by FlowJo software (version 7.6). B. CuE significantly increased the percentage of G2/M phase MDA-MB-468 cells compared to DMSO. ** p<0.01, *** p<0.001, student t-test. C. CuE significantly increased the percentage of G2/M phase SW527 cells compared to DMSO. ** p<0.01, *** p<0.001, student t-test.

Mentions: To test whether CuE modulates the cell cycle among TNBC cells, we treated MDA-MB-468 and SW527 cells with CuE at several different dosages (0, 50, 100, and 200 nM) for 24 h, after which we measured cell cycle distribution. Results showed that administration of CuE significantly increased the percentage of cells in the G2/M phase in a dosage dependent manner in both MDA-MB-468 and SW527 cell lines (Fig. 3), with the G2/M arrest induced by CuE reached its peak at 100 nM. Further increases in dosages of CuE (200 nM) did not appear to significantly increase the percentage of cells in the G2/M phase in both MDA-MB-468 and SW527 lines.


Cucurbitacin E induces cell cycle G2/M phase arrest and apoptosis in triple negative breast cancer.

Kong Y, Chen J, Zhou Z, Xia H, Qiu MH, Chen C - PLoS ONE (2014)

CuE induces cell cycle G2/M arrest in MDA-MB-468 and SW527 TNBC cell lines.A. MDA-MB-468 and SW527 cells were treated with CuE (0–50–100–200 nM) for 24 h. Cells were stained with PI and analyzed by flow cytometry. The cell cycle graph was analyzed by FlowJo software (version 7.6). B. CuE significantly increased the percentage of G2/M phase MDA-MB-468 cells compared to DMSO. ** p<0.01, *** p<0.001, student t-test. C. CuE significantly increased the percentage of G2/M phase SW527 cells compared to DMSO. ** p<0.01, *** p<0.001, student t-test.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4114842&req=5

pone-0103760-g003: CuE induces cell cycle G2/M arrest in MDA-MB-468 and SW527 TNBC cell lines.A. MDA-MB-468 and SW527 cells were treated with CuE (0–50–100–200 nM) for 24 h. Cells were stained with PI and analyzed by flow cytometry. The cell cycle graph was analyzed by FlowJo software (version 7.6). B. CuE significantly increased the percentage of G2/M phase MDA-MB-468 cells compared to DMSO. ** p<0.01, *** p<0.001, student t-test. C. CuE significantly increased the percentage of G2/M phase SW527 cells compared to DMSO. ** p<0.01, *** p<0.001, student t-test.
Mentions: To test whether CuE modulates the cell cycle among TNBC cells, we treated MDA-MB-468 and SW527 cells with CuE at several different dosages (0, 50, 100, and 200 nM) for 24 h, after which we measured cell cycle distribution. Results showed that administration of CuE significantly increased the percentage of cells in the G2/M phase in a dosage dependent manner in both MDA-MB-468 and SW527 cell lines (Fig. 3), with the G2/M arrest induced by CuE reached its peak at 100 nM. Further increases in dosages of CuE (200 nM) did not appear to significantly increase the percentage of cells in the G2/M phase in both MDA-MB-468 and SW527 lines.

Bottom Line: In this study, we compared the effects of 12 phytochemical drugs on four cancer cell lines, and noticed that Cucurbitacin E (CuE) significantly inhibited TNBC cell growth by inducing cell cycle G2/M phase arrest and apoptosis.CuE reduced expression of Cyclin D1, Survivin, XIAP, Bcl2, and Mcl-1 in MDA-MB-468 and SW527, and within MDA-MB-468, CuE significantly increased activation of JNK and inhibited activation of AKT and ERK.Collectively, these results suggest that CuE may be a viable compound for developing novel TNBC therapeutics.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, China; Kunming College of Life Science, University of Chinese Academy of Sciences, Kunming, Yunnan, China.

ABSTRACT
Triple negative breast cancer (TNBC) is a highly aggressive form of breast cancer resistant to many common treatments. In this study, we compared the effects of 12 phytochemical drugs on four cancer cell lines, and noticed that Cucurbitacin E (CuE) significantly inhibited TNBC cell growth by inducing cell cycle G2/M phase arrest and apoptosis. CuE reduced expression of Cyclin D1, Survivin, XIAP, Bcl2, and Mcl-1 in MDA-MB-468 and SW527, and within MDA-MB-468, CuE significantly increased activation of JNK and inhibited activation of AKT and ERK. Collectively, these results suggest that CuE may be a viable compound for developing novel TNBC therapeutics.

Show MeSH
Related in: MedlinePlus