| Interferon-alpha (IFN-α), as an important cytokine, exerts multiple biological activities including initiating anti-viral, anti-cancer response and immune regulatory function. The clinical observation has shown that IFN-αis one of the most effective therapeutic agents for the malignancies of hemopoietic system and lymphoma. The detailed mechanisms on the basis of anti-cancer effect of IFN-αand the resistance to IFN-αefficacy in the treatment of chronic myelogenous leukemia (CML) are not completely clear even if plenty of research has been undertaken on the level of gene and transcripts.KT-1/A3 and KT-1/A3R are two subclones of chronic myelogenous leukemia (CML) cell line KT-1, which exhibited significantly different sensitivities to the antiproliferative and apoptosis-inducing effects of IFN-α. Protein GST pi (encoded by GSTP1) was filtrated and it exhibited different expression in these two subclones, which were identified by RT-PCR and western blotting.GST pi is an important member of GSTs, which is a family of dimeric enzymes, and GST pi has been the focus of much research in recent years in relation to its involvement in the etiology of diseases, particularly cancer. The expression of GSTP 1 in the tumor tissues can be increased, decreased, and no difference in contrast to the normal tissues, so there are different mechanisms involved in effects of GSTP1 in various tumors. To understand the mechanisms involved in development and drug resistance for GSTP1 gene of CML, we have searched the proteins interacting with the GST pi in KT-1/A3R cells by "His pull-down", and have analyzed the methylation pattern of GSTP1 gene in these two subclones by MSP.We fail to find any protein interacting with the GST pi in KT-1/A3R cells because of some reasons. The results of methylation for GSTP1 gene showed that the status of methylation and non-methylation coexisted in KT-1/A3 cells, and there is only non-methylation status in KT-1/A3R cells.
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