지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2009.5
- 수록면
- 279 - 284 (6page)
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초록· 키워드
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Purpose: It is known that DNA methylation is associated with histone acetylation status in regulation of gene expression. In this study, we investigate the effect of demethylating agents and histone deacetylase (HDAC) inhibitor on the tumor suppression and the combined effect of two agents according to methylation status in human colon and breast cancer cell lines.
Methods: In this study, the RKO colorectal cancer cell line, MCF-7 breast cancer cell lines were considered. For each cell line, we used HDAC inhibitor sodium butyrate (SB), demethylating agent 5-aza-2’-deoxycytidine (5-aza-DC) and a combination of both agents. We estimated the percentage of cell survival using the XTT method and experimented with the augmentative effects of both agents.
Results: In RKO cell line in which most of the genes are methylated, 74% of cell survival was shown for 5-aza-DC treatment and 83% of cell survival for SB treatment. In MCF-7 cell line that approximately half of the genes are methylated, 82% cell survival was shown for 5-aza-DC treatment and 63% cell survival for SB treatment. We observed that the survival fraction is lower after the combined treatment of 5-aza-DC and SB than that of 5?aza?DC or SB alone in both RKO (53%) and MCF-7 (49%) cell lines (P＜0.001).
Conclusion: For highly methylated genes, 5-aza-DC is more effective on the tumor suppression than SB. On the other hand, if the methylation of the promoter region is at low density, SB is noted to be more effective than 5-aza-DC. Furthermore, the combined treatment of 5-aza-DC and SB is more effective than using each agent alone.
Methods: In this study, the RKO colorectal cancer cell line, MCF-7 breast cancer cell lines were considered. For each cell line, we used HDAC inhibitor sodium butyrate (SB), demethylating agent 5-aza-2’-deoxycytidine (5-aza-DC) and a combination of both agents. We estimated the percentage of cell survival using the XTT method and experimented with the augmentative effects of both agents.
Results: In RKO cell line in which most of the genes are methylated, 74% of cell survival was shown for 5-aza-DC treatment and 83% of cell survival for SB treatment. In MCF-7 cell line that approximately half of the genes are methylated, 82% cell survival was shown for 5-aza-DC treatment and 63% cell survival for SB treatment. We observed that the survival fraction is lower after the combined treatment of 5-aza-DC and SB than that of 5?aza?DC or SB alone in both RKO (53%) and MCF-7 (49%) cell lines (P＜0.001).
Conclusion: For highly methylated genes, 5-aza-DC is more effective on the tumor suppression than SB. On the other hand, if the methylation of the promoter region is at low density, SB is noted to be more effective than 5-aza-DC. Furthermore, the combined treatment of 5-aza-DC and SB is more effective than using each agent alone.
목차
서론
방법
결과
고찰
REFERENCES
참고문헌 (21)
참고문헌 신청
1. [학술지(정기간행물)] - Jones PA / 2002 / The fundamental role of epigenetic events in cancer / Nat Rev Genet 3 : 415 ~ 428
2. [학술지(정기간행물)] - Szyf M / 2004 / DNA methylation and breast cancer / Biochem Pharmacol 68 : 1187 ~ 1197
3. [학술지(정기간행물)] - Garinis GA / 2002 / DNA hypermethylation: when tumour suppressor genes go silent / Hum Genet 111 : 115 ~ 127
4. [학술지(정기간행물)] - Narlikar GJ / 2002 / Cooperation between complexes that regulate chromatin structure and transcription / Cell 108 : 475 ~ 487
5. [학술지(정기간행물)] - Marks P / 2001 / Histone deacetylases and cancer: causes and therapies / Nat Rev Cancer 1 : 194 ~ 202
2. [학술지(정기간행물)] - Szyf M / 2004 / DNA methylation and breast cancer / Biochem Pharmacol 68 : 1187 ~ 1197
3. [학술지(정기간행물)] - Garinis GA / 2002 / DNA hypermethylation: when tumour suppressor genes go silent / Hum Genet 111 : 115 ~ 127
4. [학술지(정기간행물)] - Narlikar GJ / 2002 / Cooperation between complexes that regulate chromatin structure and transcription / Cell 108 : 475 ~ 487
5. [학술지(정기간행물)] - Marks P / 2001 / Histone deacetylases and cancer: causes and therapies / Nat Rev Cancer 1 : 194 ~ 202
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