Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Gene expression profiles in BCL11B-siRNA treated malignant T cells. | Huang et al. Journal of Hematology Oncology 2011 4 23 http content 4 1 23 JOURNAL OF HEMATOLOGY ONCOLOGY SHORT REPORT Open Access Gene expression profiles in BCL B-siRNA treated malignant T cells 1 -z-i 1 1 I X 1 2 - 2 3 Xin Huang Qi Shen Si Chen Shaohua Chen Lijian Yang Jianyu Weng Xin Du Piotr Grabarczyk Grzegorz K Przybylski3 4 Christian A Schmidt3 and Yangqiu Li1 5 Abstract Background Downregulation of the B-cell chronic lymphocytic leukemia CLL lymphoma11B BCL11B gene by small interfering RNA siRNA leads to growth inhibition and apoptosis of the human T-cell acute lymphoblastic leukemia T-ALL cell line Molt-4. To further characterize the molecular mechanism a global gene expression profile of BCL11B-siRNA -treated Molt-4 cells was established. The expression profiles of several genes were further validated in the BCL11B-siRNA -treated Molt-4 cells and primary T-ALL cells. Results 142 genes were found to be upregulated and 109 genes downregulated in the BCL11B-siRNA -treated Molt-4 cells by microarray analysis. Among apoptosis-related genes three pro-apoptotic genes TNFSF10 BIK BNIP3 were upregulated and one anti-apoptotic gene BCL2L1 was downregulated. Moreover the expression of SPP1 and CREBBP genes involved in the transforming growth factor TGF P pathway was down 16-fold. Expression levels of TNFSF10 BCL2L1 SPP1 and CREBBP were also examined by real-time PCR. A similar expression pattern of TNFSF10 BCL2L1 and SPP1 was identified. However CREBBP was not downregulated in the BLC11B-siRNA -treated Molt-4 cells. Conclusion BCL11B-siRNA treatment altered expression profiles of TNFSF10 BCL2L1 and SPP1 in both Molt-4 T cell line and primary T-ALL cells. Background Although treatment outcome in patients with T-cell acute lymphoblastic leukemia T-ALL has improved in recent years relapsed T-ALL remains a challenge 1 . Monoclonal antibodies gene inhibitors and upregulation of microRNAs 2 3 are promising tools for cancer targeted therapy. However .
