지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2009.11
- 수록면
- 297 - 305 (9page)
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Purpose: The causes of colon cancer can be divided into genetic and environmental components. A high-fiber diet is known to reduce the risk of colon cancer. Dietary fiber is converted to short chain fatty acid, butyrate, in the colon by bacteria. Butyrate is used as an energy source for the colonic epithelial cells, and is known to induce apoptosis in colon cancer cell lines. Survivin, a recently discovered member of the IAP (inhibitor of apoptosis) family, is known to suppress apoptosis. Not only does it suppress cell apoptosis, but it also has a protective effect from disabling G2/M phase of the cell cycle by attaching to the microtubule of the mitotic spindle. The purpose of this study is to evaluate the effect of butyrate on the expression of survivin, in HCT116 colon cancer cell lines.
Methods: Cytotoxicity of butyrate was measured by MTS method. Cell cycle phase and apoptosis was analyzed by flowcytometry. Protein expression of survivin was evaluated by Western blot analysis, and the mRNA expression by RT-PCR.
Results: Butyrate can induce apoptosis in HCT116 colon cancer cell line at a concentration of 6 mM. Butyrate suppressed the expression of survivin mRNA and also the expression of cytosolic and nuclear survivin. In flowcytometric analysis, the apoptotic portion was increased and the proportions of S and M phase were decreased when cultured with butyrate.
Conclusion: We concluded that butyrate could induce cellular apoptosis partially by suppressing the expression of survivin in HCT116 colon cancer cells.
Methods: Cytotoxicity of butyrate was measured by MTS method. Cell cycle phase and apoptosis was analyzed by flowcytometry. Protein expression of survivin was evaluated by Western blot analysis, and the mRNA expression by RT-PCR.
Results: Butyrate can induce apoptosis in HCT116 colon cancer cell line at a concentration of 6 mM. Butyrate suppressed the expression of survivin mRNA and also the expression of cytosolic and nuclear survivin. In flowcytometric analysis, the apoptotic portion was increased and the proportions of S and M phase were decreased when cultured with butyrate.
Conclusion: We concluded that butyrate could induce cellular apoptosis partially by suppressing the expression of survivin in HCT116 colon cancer cells.
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방법
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고찰
REFERENCES
참고문헌 (29)
참고문헌 신청
1. [학술지(정기간행물)] - Hague A / 1993 / Sodium butyrate induces apoptosis in human colonic tumour cell lines in a p53-independent pathway: implications for the possible role of dietary fibre in the prevention of large-bowel cancer / Int J Cancer 55 : 498 ~ 505
2. [학술지(정기간행물)] - Bonnotte B / 1998 / Cancer cell sensitization to fas-mediated apoptosis by sodium butyrate / Cell Death Differ 5 : 480 ~ 487
3. [학술지(정기간행물)] - Giardina C / 1999 / NSAIDs and butyrate sensitize a human colorectal cancer cell line to TNF-alpha and Fas ligation: the role of reactive oxygen species / Biochim Biophys Acta 1448 : 425 ~ 438
4. [학술지(정기간행물)] - McMillan L / 2003 / Opposing effects of butyrate and bile acids on apoptosis of human colon adenoma cells: differential activation of PKC and MAP kinases / Br J Cancer 88 : 748 ~ 753
5. [학술지(정기간행물)] - Sandler RS / 1993 / Diet and risk of colorectal adenomas: macronutrients, cholesterol, and fiber / J Natl Cancer Inst 85 : 884 ~ 891
2. [학술지(정기간행물)] - Bonnotte B / 1998 / Cancer cell sensitization to fas-mediated apoptosis by sodium butyrate / Cell Death Differ 5 : 480 ~ 487
3. [학술지(정기간행물)] - Giardina C / 1999 / NSAIDs and butyrate sensitize a human colorectal cancer cell line to TNF-alpha and Fas ligation: the role of reactive oxygen species / Biochim Biophys Acta 1448 : 425 ~ 438
4. [학술지(정기간행물)] - McMillan L / 2003 / Opposing effects of butyrate and bile acids on apoptosis of human colon adenoma cells: differential activation of PKC and MAP kinases / Br J Cancer 88 : 748 ~ 753
5. [학술지(정기간행물)] - Sandler RS / 1993 / Diet and risk of colorectal adenomas: macronutrients, cholesterol, and fiber / J Natl Cancer Inst 85 : 884 ~ 891
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UCI(KEPA) : I410-ECN-0101-2013-514-002680940