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초청세미나

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종양연구소 초청세미나 (2015.02.27)
종양연구소 조회수:417
2017-05-18 15:58:25

충북대학교 종양연구소에서 다음과 같이 초청세미나를 개최하오니 많은 참여 부탁드립니다.

                                         - 다 음 -

1. 연 자 :  현 진 원 교수 (제주대학교)

2. 일 시 :  2015년 02월 27일 (금) 오후 3시

3. 연 제 :  Epigenetic change induced by oxidative stress in colorectal cancer cell

                : methylation of tumor suppressor RUNX3

4. 장 소 : 종양연구소 세미나실 104호

5. 발 표 내 용 

 

Runt domain transcription factor 3 (RUNX3) is a tumor suppressor that is silenced in cancer via hypermethylation of its promoter. This study investigated mechanisms involved in reactive oxygen species (ROS)-induced silencing of RUNX3 in terms of epigenetic alteration, since the effects of oxidative stress in tumor suppressor gene transcription are largely unknown. RUNX3 mRNA and protein expressions were down-regulated in response to hydrogen peroxide (H2O2) in the human colorectal cancer cell line SNU-407. This down-regulation was abolished with pretreatment of the ROS scavenger, N-acetylcysteine (NAC). Moreover, methylation specific PCR data revealed that H2O2 treatment increased RUNX3 promoter methylation, however, NAC and the cytosine methylation inhibitor, 5-aza-2-deoxycytidine, decreased it, suggesting that an epigenetic regulatory mechanism by ROS-induced methylation may be involved in RUNX3 silencing. H2O2 treatment resulted in DNMT1 and HDAC1 up-regulation with increased expression and activity, increased binding of DNMT1 to HADC1, and increased DNMT1 binding to the RUNX3 promoter. In addition, 5-Aza-dC treatment prevented the decrease in RUNX3 mRNA and protein levels by H2O2 treatment. Additionally, H2O2 treatment inhibited the nuclear localization and expression of RUNX3, which was abolished by NAC treatment. Taken together, the data suggested that ROS silence the tumor suppressor, RUNX3, by epigenetic regulation and may therefore be associated with the progression of colorectal cancer.

 

 

 

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