| Title | E1AF promotes mithramycin A-induced Huh-7 cell apoptosis depending on its DNA-binding domain. | | Author(s) | Liu D, Wei Y, Zhou F, Ge Y, Xu J, Chen H, Zhang W, Yun X, Jiang J | | Institution | Key Laboratory of Glycoconjugates Research, Ministry of Public Health & Gene Research Center, Shanghai Medical College of Fudan University, Dongan Road 130, Shanghai 200032, People’s Republic of China. | | Source | Arch Biochem Biophys 2008 May 14. | | Abstract | Transcription factor E1AF is widely known to play critical roles in tumor metastasis via directly binding to the promoters of genes involved in tumor migration and invasion. Here, we reported for the first time the pro-apoptotic role of E1AF in tumor cells. The expression of E1AF at protein level was obviously increased during Huh-7 and Hep3B cells apoptosis induced by the anticancer agent mithramycin A. E1AF overexpression markedly enhanced mithramycin A-induced Huh-7 cell apoptosis and the expression of pro-apoptotic protein Bax depending on its DNA-binding domain. And, reduction of E1AF inhibited mithramycin A-induced Huh-7 cell apoptosis. Furthermore, reducing the expression of Bax significantly inhibited E1AF-increased Huh-7 cell apoptosis induced by mithramycin A. Taken together, E1AF increases mithramycin A-induced Huh-7 cells apoptosis and Bax expression depending on its DNA-binding domain, indicating that E1AF might contribute to the therapeutic efficiency of mithramycin A for hepatoma. | | Language | ENG | | Pub Type(s) | JOURNAL ARTICLE
| | PubMed ID | 18510939 |
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