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Cucurbitacin B Causes Increased Radiation Sensitivity of Human Breast Cancer Cells via G2/M Cell Cycle Arrest.

Duangmano S, Sae-Lim P, Suksamrarn A, Patmasiriwat P, Domann FE - J Oncol (2012)

Bottom Line: Results.Flow cytometric analysis for DNA content indicated that cucurbitacin B resulted in G2/M arrest in MDA-MB-231 and MCF7:5C but not SKBR-3 cells.Therefore, combinations of cucurbitacin B with radiotherapy may be appropriate for experimental breast cancer treatment.

View Article: PubMed Central - PubMed

Affiliation: Faculty of Medical Technology, Mahidol University, Bangkok, Thailand.

ABSTRACT
Purpose. To explore the effects of cucurbitacin B on the radiation survival of human breast cancer cells and to elucidate the cellular mechanism of radiosensitization if any. Materials and Methods. Human breast carcinoma cell lines were treated with cucurbitacin B before irradiation with 0-10 Gy of (137)Cs gamma rays. The effect of cucurbitacin B on cell-survival following irradiation was evaluated by colony-forming assay. Cell cycle distributions were investigated using flow cytometry. Real-time PCR and western blots were performed to investigate the expression of cell cycle checkpoints. Results. Cucurbitacin B inhibited breast cancer cell proliferation in a dose-dependent manner. Only MDA-MB-231 and MCF7:5C cells but not SKBR-3 cells were radiosensitized by cucurbitacin B. Flow cytometric analysis for DNA content indicated that cucurbitacin B resulted in G2/M arrest in MDA-MB-231 and MCF7:5C but not SKBR-3 cells. Moreover, Real-time PCR and western blot analysis demonstrated upregulated p21 expression before irradiation, a likely cause of the cell cycle arrest. Conclusion. Taken together, these findings suggest that cucurbitacin B causes radiosensitization of some breast cancer cells, and that cucurbitacin B induced G2/M arrest is an important mechanism. Therefore, combinations of cucurbitacin B with radiotherapy may be appropriate for experimental breast cancer treatment.

No MeSH data available.


Related in: MedlinePlus

The inhibitory effects of cucurbitacin B on colony formation in breast cancer cells. MCF7:5C, MDA-MB-231, and SKBR-3 were treated with the indicated concentration of cucurbitacin B for 48 hr. After incubating, cells were seeded on the basis of difference density in a 60 mm culture plate with 5 mL of fresh medium. At 14 days after seeding, colonies were fixed and stained with 0.1% crystal violet. Results shown are the average of three independent experiments. *P < 0.05 versus nontreated control, **P < 0.01 versus nontreated control.
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fig1: The inhibitory effects of cucurbitacin B on colony formation in breast cancer cells. MCF7:5C, MDA-MB-231, and SKBR-3 were treated with the indicated concentration of cucurbitacin B for 48 hr. After incubating, cells were seeded on the basis of difference density in a 60 mm culture plate with 5 mL of fresh medium. At 14 days after seeding, colonies were fixed and stained with 0.1% crystal violet. Results shown are the average of three independent experiments. *P < 0.05 versus nontreated control, **P < 0.01 versus nontreated control.

Mentions: The inhibitory effect of cucurbitacin B on colony formation in human breast cancer cells was evaluated by clonogenic assay. Cells were incubated with cucurbitacin B alone for 48 hr and then allowed to form colonies in fresh medium. The surviving fraction as a function of drug concentration is shown in Figure 1. The average 50% (IC50) inhibitory concentrations for clonogenic cell death in three cells was 3.2, 2.4, and 1.9 μM for MCF7:5C, and MDA-MB-231, and SKBR-3 respectively. The results are the average from three independent experiments for each cell lines. In the clonogenic assay SKBR-3, was the most sensitive cell to cucurbitacin B under the same condition for other cells.


Cucurbitacin B Causes Increased Radiation Sensitivity of Human Breast Cancer Cells via G2/M Cell Cycle Arrest.

Duangmano S, Sae-Lim P, Suksamrarn A, Patmasiriwat P, Domann FE - J Oncol (2012)

The inhibitory effects of cucurbitacin B on colony formation in breast cancer cells. MCF7:5C, MDA-MB-231, and SKBR-3 were treated with the indicated concentration of cucurbitacin B for 48 hr. After incubating, cells were seeded on the basis of difference density in a 60 mm culture plate with 5 mL of fresh medium. At 14 days after seeding, colonies were fixed and stained with 0.1% crystal violet. Results shown are the average of three independent experiments. *P < 0.05 versus nontreated control, **P < 0.01 versus nontreated control.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3368438&req=5

fig1: The inhibitory effects of cucurbitacin B on colony formation in breast cancer cells. MCF7:5C, MDA-MB-231, and SKBR-3 were treated with the indicated concentration of cucurbitacin B for 48 hr. After incubating, cells were seeded on the basis of difference density in a 60 mm culture plate with 5 mL of fresh medium. At 14 days after seeding, colonies were fixed and stained with 0.1% crystal violet. Results shown are the average of three independent experiments. *P < 0.05 versus nontreated control, **P < 0.01 versus nontreated control.
Mentions: The inhibitory effect of cucurbitacin B on colony formation in human breast cancer cells was evaluated by clonogenic assay. Cells were incubated with cucurbitacin B alone for 48 hr and then allowed to form colonies in fresh medium. The surviving fraction as a function of drug concentration is shown in Figure 1. The average 50% (IC50) inhibitory concentrations for clonogenic cell death in three cells was 3.2, 2.4, and 1.9 μM for MCF7:5C, and MDA-MB-231, and SKBR-3 respectively. The results are the average from three independent experiments for each cell lines. In the clonogenic assay SKBR-3, was the most sensitive cell to cucurbitacin B under the same condition for other cells.

Bottom Line: Results.Flow cytometric analysis for DNA content indicated that cucurbitacin B resulted in G2/M arrest in MDA-MB-231 and MCF7:5C but not SKBR-3 cells.Therefore, combinations of cucurbitacin B with radiotherapy may be appropriate for experimental breast cancer treatment.

View Article: PubMed Central - PubMed

Affiliation: Faculty of Medical Technology, Mahidol University, Bangkok, Thailand.

ABSTRACT
Purpose. To explore the effects of cucurbitacin B on the radiation survival of human breast cancer cells and to elucidate the cellular mechanism of radiosensitization if any. Materials and Methods. Human breast carcinoma cell lines were treated with cucurbitacin B before irradiation with 0-10 Gy of (137)Cs gamma rays. The effect of cucurbitacin B on cell-survival following irradiation was evaluated by colony-forming assay. Cell cycle distributions were investigated using flow cytometry. Real-time PCR and western blots were performed to investigate the expression of cell cycle checkpoints. Results. Cucurbitacin B inhibited breast cancer cell proliferation in a dose-dependent manner. Only MDA-MB-231 and MCF7:5C cells but not SKBR-3 cells were radiosensitized by cucurbitacin B. Flow cytometric analysis for DNA content indicated that cucurbitacin B resulted in G2/M arrest in MDA-MB-231 and MCF7:5C but not SKBR-3 cells. Moreover, Real-time PCR and western blot analysis demonstrated upregulated p21 expression before irradiation, a likely cause of the cell cycle arrest. Conclusion. Taken together, these findings suggest that cucurbitacin B causes radiosensitization of some breast cancer cells, and that cucurbitacin B induced G2/M arrest is an important mechanism. Therefore, combinations of cucurbitacin B with radiotherapy may be appropriate for experimental breast cancer treatment.

No MeSH data available.


Related in: MedlinePlus