Id-1 regulates Bcl-2 and Bax expression through p53 and NF-kappa B in MCF-7 breast cancer cells
DC Field | Value | Language |
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dc.contributor.author | Kim, Hwan | - |
dc.contributor.author | Chung, Heekyoung | - |
dc.contributor.author | Kim, Hyun-Jun | - |
dc.contributor.author | Lee, Jeong-Yeon | - |
dc.contributor.author | Oh, Mi-Yun | - |
dc.contributor.author | Kim, Yongseok | - |
dc.contributor.author | Kong, Gu | - |
dc.date.accessioned | 2022-10-07T09:46:01Z | - |
dc.date.available | 2022-10-07T09:46:01Z | - |
dc.date.created | 2022-08-26 | - |
dc.date.issued | 2008-11 | - |
dc.identifier.issn | 0167-6806 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/171789 | - |
dc.description.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. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | SPRINGER | - |
dc.title | Id-1 regulates Bcl-2 and Bax expression through p53 and NF-kappa B in MCF-7 breast cancer cells | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Chung, Heekyoung | - |
dc.contributor.affiliatedAuthor | Lee, Jeong-Yeon | - |
dc.contributor.affiliatedAuthor | Kim, Yongseok | - |
dc.contributor.affiliatedAuthor | Kong, Gu | - |
dc.identifier.doi | 10.1007/s10549-007-9871-6 | - |
dc.identifier.scopusid | 2-s2.0-53949096318 | - |
dc.identifier.wosid | 000260064400008 | - |
dc.identifier.bibliographicCitation | BREAST CANCER RESEARCH AND TREATMENT, v.112, no.2, pp.287 - 296 | - |
dc.relation.isPartOf | BREAST CANCER RESEARCH AND TREATMENT | - |
dc.citation.title | BREAST CANCER RESEARCH AND TREATMENT | - |
dc.citation.volume | 112 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 287 | - |
dc.citation.endPage | 296 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Oncology | - |
dc.relation.journalWebOfScienceCategory | Oncology | - |
dc.subject.keywordPlus | PROSTATE-CANCER | - |
dc.subject.keywordPlus | TRANSCRIPTION FACTOR | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | INTERLEUKIN-6 GENE | - |
dc.subject.keywordPlus | SIGNALING PATHWAY | - |
dc.subject.keywordPlus | INDUCED APOPTOSIS | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | METASTASIS | - |
dc.subject.keywordPlus | INHIBITOR | - |
dc.subject.keywordPlus | PROTEINS | - |
dc.subject.keywordAuthor | Id-1 | - |
dc.subject.keywordAuthor | apoptosis | - |
dc.subject.keywordAuthor | p53 | - |
dc.subject.keywordAuthor | NF-kappa B | - |
dc.subject.keywordAuthor | Bax | - |
dc.subject.keywordAuthor | Bcl-2 | - |
dc.identifier.url | Alzheimer Disease; Amyloid beta-Protein; Animals; Caspase 3; Cell Survival; Cells, Cultured; Coloring Agents; Cytochromes c; DNA-Binding Proteins; Dose-Response Relationship, Drug; Enzyme Activation; Enzyme Inhibitors; Glycogen Synthase Kinase 3; Indicators and Reagents; Nerve Degeneration; Neurons; Neurotoxins; Peptide Fragments; Rats; Rats, Sprague-Dawley; Signal Transduction; tau Proteins; Tetrazolium Salts; Transcription Factors | - |
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