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RISS 인기검색어
- 검색키워드
- 저자 : Dingyun You (검색결과 2 건)
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Acetylation Enhances the Promoting Role of AIB1 in Breast Cancer Cell Proliferation
You, Dingyun,Zhao, Hongbo,Wang, Yan,Jiao, Yang,Lu, Minnan,Yan, Shan Korean Society for Molecular and Cellular Biology 2016 Molecules and cells Vol.39 No.9
The oncogene nuclear receptor coactivator amplified in breast cancer 1 (AIB1) is a transcriptional coactivator, which is overexpressed in various types of human cancers, including breast cancer. However, the molecular mechanisms regulating AIB1 function remain largely unknown. In this study, we present evidence demonstrating that AIB1 is acetylated by MOF in human breast cancer cells. Moreover, we also found that the acetylation of AIB1 enhances its function in promoting breast cancer cell proliferation. We further showed that the acetylation of AIB1 is required for its recruitment to E2F1 target genes by E2F1. More importantly, we found that the acetylation levels of AIB1 are greatly elevated in human breast cancer cells compared with that in non-cancerous cells. Collectively, our results shed light on the molecular mechanisms that regulate AIB1 function in breast cancer.
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Acetylation Enhances the Promoting Role of AIB1 in Breast Cancer Cell Proliferation
Shan Yan,Dingyun You,Hongbo Zhao,Yan Wang,Yang Jiao,Minnan Lu 한국분자세포생물학회 2016 Molecules and cells Vol.39 No.9
The oncogene nuclear receptor coactivator amplified in breast cancer 1 (AIB1) is a transcriptional coactivator, which is overexpressed in various types of human cancers, including breast cancer. However, the molecular mechanisms regulating AIB1 function remain largely unknown. In this study, we present evidence demonstrating that AIB1 is acetylated by MOF in human breast cancer cells. Moreover, we also found that the acetylation of AIB1 enhances its function in promoting breast cancer cell proliferation. We further showed that the acetylation of AIB1 is required for its recruitment to E2F1 target genes by E2F1. More importantly, we found that the acetylation levels of AIB1 are greatly elevated in human breast cancer cells compared with that in non-cancerous cells. Collectively, our results shed light on the molecular mechanisms that regulate AIB1 function in breast cancer.
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