3, 3′5 triiodo l thyronine induces apoptosis in human breast cancer mcf-7cells, repressing smp30 expression through negative thyroid response elements3、3u20325 l三碘甲状腺原氨酸人类乳腺癌mcf-7cells发生凋亡,抑制smp30表达式通过负甲状腺响应元素.pdfVIP

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3, 3′5 triiodo l thyronine induces apoptosis in human breast cancer mcf-7cells, repressing smp30 expression through negative thyroid response elements3、3u20325 l三碘甲状腺原氨酸人类乳腺癌mcf-7cells发生凋亡,抑制smp30表达式通过负甲状腺响应元素.pdf

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3, 3′5 triiodo l thyronine induces apoptosis in human breast cancer mcf-7cells, repressing smp30 expression through negative thyroid response elements3、3u20325 l三碘甲状腺原氨酸人类乳腺癌mcf-7cells发生凋亡,抑制smp30表达式通过负甲状腺响应元素

3, 395 Triiodo L Thyronine Induces Apoptosis in Human Breast Cancer MCF-7cells, Repressing SMP30 Expression through Negative Thyroid Response Elements 1 1 1 2 1 Pranati Sar , Rosalima Peter , Bandita Rath , Alok Das Mohapatra , Sandip K. Mishra * 1 Cancer Biology Lab, Department of Gene Function and Regulation, Institute of Life Sciences, Chandrasekharpur, Bhubaneswar, India, 2 Vector Born Disease Lab, Department of Infectious Disease Biology, Institute of Life Sciences, Chandrasekharpur, Bhubaneswar, India Abstract Background: Thyroid hormones regulate cell proliferation, differentiation as well as apoptosis. However molecular mechanism underlying apoptosis as a result of thyroid hormone signaling is poorly understood. The antiapoptotic role of Senescence Marker Protein-30 (SMP30) has been characterized in response to varieties of stimuli as well as in knock out model. Our earlier data suggest that thyroid hormone 3, 395 Triiodo L Thyronine (T3), represses SMP30 in rat liver. Methodology/Principal Findings: In highly metastatic MCF-7, human breast cancer cell line T3 treatment repressed SMP30 expression leading to enhanced apoptosis. Analysis by flow cytometry and other techniques revealed that overexpression and silencing of SMP30 in MCF-7 resulted in decelerated and accelerated apoptosis respectively. In order to identify the cis– acting elements involved in this regulation, we have analyzed hormone responsiveness of transiently transfected hSMP30 promoter deletion reporter vectors in MCF-7 cells. As opposed to the expected epigenetic outcome, thyroid hormone down regulated hSMP30 promoter activity despite enhanced recruitment of acetylated H3 on thyroid response elements (TREs). From the stand poin