ABSTRACT
Objective To investigate and clarify the effect of Stat5a on proliferation of human breast cancer cells (MCF‐7) and to detect the changes of epigenetic signature on the promoter region of p53 gene .Methods Stat5a was over expressed in human breast cancer cells (MCF‐7) by using adenovirus mediated gene transfer technology .The cell proliferation was examined by MTS assay .ChIP assay was used to check the trimethylation of lysine 27 on histone 3 (H3K27Me3) of p53 gene promoter region .Fur‐thermore ,qRT‐PCR and western blot were also applied to confirm the expression of p53 gene .Results The number of MCF 7 in‐creased in a dose dependent manner .Compared with that of control group ,the cell density of MCF‐7 increased 7 .603 1% , 18 .123 7% and 24 .898 7% when the MOI were 10 ,20 and 30 .Chromatin Immunoprecipitation showed that Stat5a significantly in‐creased H3K27Me3 and down regulated the expression level of p53 gene .Conclusion Stat5a promotes proliferation of breast cancer cells through trimethylation of H3K27 and inhibition of p53 gene expression .
ABSTRACT
PURPOSE: To investigate the role of STAT5 during osteogenesis differentiation of human mesenchymal stem cells(hMSC). MATERIALS AND METHODS: To assess the expression pattern of STATs during osteogenic differentiation, we performed western blot analysis and RT-PCR. By RNA interference, we have performed effect of STAT5A and STAT5B in osteogenesis. As a result of Luciferase assay, the promoter activity of DLX5 was decreased by STAT5A. RESULTS: To assess the expression pattern of STATs during osteogenic differentiation, we have performed western blot and RT-PCR after 14 day differentiation period. STAT1, 2, 3 and 4 showed no change in expression level during differentiation, while STAT5A and STAT5B displayed steady increase compared to the control. When STAT5A was knock down, the level of osteogenesis was increased. The transcriptional activity of DLX5 was decreased about 70% by STAT5A. CONCLUSION: The expression of STAT5A and STAT5B increased during osteogenesis of hMSC. Also, we shown that STAT5A regulated the transcriptional activity of DLX5. These results indicate that STAT5A acts as a pivotal transcription factor in osteogenesis of hMSC.