Id-1 regulates Bcl-2 and Bax expression through p53 and NF-kappa B in MCF-7 breast cancer cells
- Authors
- Kim, Hwan; Chung, Heekyoung; Kim, Hyun-Jun; Lee, Jeong-Yeon; Oh, Mi-Yun; Kim, Yongseok; Kong, Gu
- Issue Date
- Nov-2008
- Publisher
- SPRINGER
- Keywords
- Id-1; apoptosis; p53; NF-kappa B; Bax; Bcl-2
- Citation
- BREAST CANCER RESEARCH AND TREATMENT, v.112, no.2, pp.287 - 296
- Indexed
- SCIE
SCOPUS
- Journal Title
- BREAST CANCER RESEARCH AND TREATMENT
- Volume
- 112
- Number
- 2
- Start Page
- 287
- End Page
- 296
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/171789
- DOI
- 10.1007/s10549-007-9871-6
- ISSN
- 0167-6806
- Abstract
- Although increasing evidence supports the protective role of inhibitor of differentiation and DNA binding-1 (Id-1) against anticancer drug-induced apoptosis, the underlying molecular mechanisms seem to vary depending on the tumor system. Here, we examined the direct role of Id-1 in MCF-7 breast cancer cells by ectopically overexpressing Id-1 under serum-free condition, where the endogenous Id-1 expression was suppressed. Id-1 expression resulted in increased number of viable cells, reduced Bax expression, enhanced Bcl-2 expression, but no change in Bcl-xL expression. The expression of nuclear factor-kappa B (NF-kappa B) was augmented, while those of p53 and I kappa B were reduced. Such changes in p53 and NF-kappa B pathways were also functional, as assessed by real-time polymerase chain reactions and reporter assays of their known downstream targets, p21 and Il-6, as well as Bax and Bcl-2 genes. Finally, Id-1 played a protective role against taxol-induced apoptosis in breast cancer cells as assessed by MTT assay and apoptotic cell count upon taxol treatment (0-200 nM). Reduced Bax expression and enhanced Bcl-2 expression by Id-1 were also noted in the presence of taxol. Taken together, we present a molecular mechanism where Id-1 regulates p53 and NF-kappa B pathways, which in turn regulates Bax and Bcl-2 genes, thus providing a survival advantage under exogenous stress such as serum-free or taxol treatment in MCF-7 breast cancer cells. In this regard, inactivation of Id-1 may provide a potential therapeutic strategy leading to inhibition of breast cancer progression and anti-cancer drug resistance.
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