http://www.bioscirep.org Bioscience Reports RSS feed -- Immediate Publications 0144-8463 1573-4935 Bioscience Reports http://www.bioscirep.org/images/BSR_PDF_Icon.jpg http://www.bioscirep.org http://www.bioscirep.org/bsr/imps/refer.htm?MSID=BSR20110045 pdcd4 promoter, a functional CCAAT-box, and the basal promoter region. Within this basal region, computer-based analysis revealed several potential binding sites for zinc finger binding proteins, especially for Sp-family members and ZBP-89. We identified four Sp1/Sp3/Sp4 binding elements to be indispensable for basal promoter activity. However, overexpression of Sp1 and Sp3 was not sufficient to enhance Pdcd4 protein expression. Analysis in different solid cancer cell lines showed a significant correlation between pdcd4 and zbp-89 mRNA amounts. In contrast to Sp transcription factors, overexpression of ZBP-89 led to an enhanced expression of Pdcd4 mRNA and protein. Additionally, specific knockdown of ZBP-89 resulted in a decreased pcdcd4 gene expression. Reporter gene analysis showed a significant upregulation of basal promoter activity by cotransfection with ZBP-89, which could be abolished by mithramycin treatment. Predicted binding of ZBP-89 to the basal promoter was confirmed by EMSA data, supershift analysis for ZBP-89. Taken together, data for the first time implicate ZBP-89 as a regulator of Pdcd4 by binding to the basal promoter either alone or by interacting with Sp-family members.]]> J Hendrik Leupold, I Ahmed Asangani, G Mudduluru, H Allgayer 2011-11-23T15:31:44Z doi:10.1042/BSR20110045 Portland Press Limited 2011-11-23 http://www.bioscirep.org/bsr/imps/refer.htm?MSID=BSR20110033 E. coli. Immunofluorescence staining and Western blot were performed to identify the expression and internalization of TAT-FHIT in hepatocellular carcinoma cells compared with the purified FHIT protein. Our study showed that TAT-FHIT protein can translocate into cancer cells in one hour after incubation in 37℃. Furthermore, the results of MTT assay, Annexin-V staining and Western blot demonstrated that TAT-FHIT can robustly inhibit growth and induce apoptosis of hepatocellular cancer cells in vitro. In addition, mechanistic study showed that both exogenous and intrinsic apoptotic pathways were involved in TAT-FHIT-mediated apoptosis and this effect could be attenuated partially by a mitochondrial protector TAT-BH4, indicating that mitochondria plays a critical role in TAT-FHIT-mediated pro-apoptotic effect in cancer cells. Taken together, our study suggests that TAT-FHIT is a potential pro-apoptotic molecule in hepatocellular cancer cells and strengthen the hypothesis of its therapeutic application against hepatocellular carcinoma.]]> G Yu, W Qin, J Li, W Hua, Y Meng, R Chen, B Yan, L Wang, X Zhang, L Jia, J Zhao, r zhang, A Yang 2011-06-16T12:37:20Z doi:10.1042/BSR20110033 Portland Press Limited 2011-06-16