SAHA treatment overcomes the anti-apoptotic effects of Bcl-2 and is associated with the formation of mature PML nuclear bodies in human leukemic U937 cells

Title
SAHA treatment overcomes the anti-apoptotic effects of Bcl-2 and is associated with the formation of mature PML nuclear bodies in human leukemic U937 cells
Authors
Jee Suk LeeSeung Hun JeongYoung Hwa SoungTae Hyun KimHong Jo ChoiBong Soo ParkTaeg Kyu KwonYoung Hyun Yoo
Keimyung Author(s)
권택규
Department
Dept. of Immunology (면역학); Chronic Disease Research Center (만성 질환 연구 센터); Institute for Medical Science (의과학연구소)
Issue Date
2009
Publisher
School of Medicine
Citation
Chemico-Biological Interactions, Vol.181(1) : 61-70, 2009
Abstract
Bcl-2 protects tumor cells from the apoptotic effects of various antineoplastic agents. Increased expression of Bcl-2 has been associated with poor response to chemotherapy in various malignancies, including leukemia. Therefore, bypassing the resistance conferred by anti-apoptotic factors such as Bcl-2 represents an attractive therapeutic strategy against cancer cells, including leukemic cells. We undertook this study to examine whether SAHA (suberoylanilide hydroxamic acid) overcomes the resistance by Bcl-2 in human leukemic cells, with a specific focus on the involvement of PML-NBs. Experiments were conducted with Bcl-2-overexpressing human leukemic U937 cells. Since we previously demonstrated that overexpression of Bcl-2 attenuates resveratrol-induced apoptosis in human leukemic U937 cells, resveratrol-treated U937 cells were used as a negative control. The present study indicates that SAHA at 1–7 μM, the dose range known to induce apoptosis in various cancer cells, overcomes the anti-apoptotic effects of Bcl-2 in Bcl-2-overexpressing human leukemic U937 cells. Notably, we observed that SAHA-induced formation of mature promyelocytic leukemia (PML) nuclear bodies (NBs) correlates with overcoming the anti-apoptotic effects of Bcl-2 in human leukemic U937 cells. Thus, PML protein and the formation of mature PML-NBs could be considered as therapeutic targets that could help bypass the resistance to apoptosis conferred by Bcl-2. Elucidating exactly how PML regulates Bcl-2 will require further work.
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/17055
ISSN
0009-2797
Appears in Collections:
1. 연구논문 > 3. Researcher Institutues (부설연구소) > Chronic Disease Research Center (만성질환연구센터)
1. 연구논문 > 3. Researcher Institutues (부설연구소) > Institute for Medical Science (의과학연구소)
1. 연구논문 > 1. School of Medicine (의과대학) > Dept. of Immunology (면역학)
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