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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

Effect of cucurbitacin B on the cell cycle progression of breast cancer cells. MCF7:5C, MDA-MB-231, and SKBR-3 were treated with cucurbitacin B for 48 hr, and then stained with propidium iodide (PI) and subjected to flow cytometric analysis. The DNA histograms shown are representative of three independent experiments. Blockage at G2/M and apoptotic induction was observed (SubG1).
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fig2: Effect of cucurbitacin B on the cell cycle progression of breast cancer cells. MCF7:5C, MDA-MB-231, and SKBR-3 were treated with cucurbitacin B for 48 hr, and then stained with propidium iodide (PI) and subjected to flow cytometric analysis. The DNA histograms shown are representative of three independent experiments. Blockage at G2/M and apoptotic induction was observed (SubG1).

Mentions: Effect of cucurbitacin B on cell cycle progression in MCF7:5C, MDA-MB-231, and SKBR-3 cells were analyzed according to the principle of the DNA content in each phase of, cell cycle. Cells were treated with cucurbitacin B for 48 hr, and DNA content was analyzed via flow cytometry. MCF7:5C and MDA-MB-231 cells after treated were arrested at G2/M phase of cell cycle with a decrease of cells population in G1 and S phase of cell cycle, as was observed in several cancer cell lines. However, in contrast to the effect of cucurbitacin B on MCF7:5C and MDA-MB-231 cells, cucurbitacin B did not contribute to G2/M phase arrest in SKBR-3 cells (Figure 2).


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)

Effect of cucurbitacin B on the cell cycle progression of breast cancer cells. MCF7:5C, MDA-MB-231, and SKBR-3 were treated with cucurbitacin B for 48 hr, and then stained with propidium iodide (PI) and subjected to flow cytometric analysis. The DNA histograms shown are representative of three independent experiments. Blockage at G2/M and apoptotic induction was observed (SubG1).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig2: Effect of cucurbitacin B on the cell cycle progression of breast cancer cells. MCF7:5C, MDA-MB-231, and SKBR-3 were treated with cucurbitacin B for 48 hr, and then stained with propidium iodide (PI) and subjected to flow cytometric analysis. The DNA histograms shown are representative of three independent experiments. Blockage at G2/M and apoptotic induction was observed (SubG1).
Mentions: Effect of cucurbitacin B on cell cycle progression in MCF7:5C, MDA-MB-231, and SKBR-3 cells were analyzed according to the principle of the DNA content in each phase of, cell cycle. Cells were treated with cucurbitacin B for 48 hr, and DNA content was analyzed via flow cytometry. MCF7:5C and MDA-MB-231 cells after treated were arrested at G2/M phase of cell cycle with a decrease of cells population in G1 and S phase of cell cycle, as was observed in several cancer cell lines. However, in contrast to the effect of cucurbitacin B on MCF7:5C and MDA-MB-231 cells, cucurbitacin B did not contribute to G2/M phase arrest in SKBR-3 cells (Figure 2).

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