Regulation of Insulin-like Growth Factor II P3 Promoter by p53: A Potential Mechanism for Tumorigenesis
作者： Lijuan Zhang , Fatah Kashanchi , Qimin Zhan , Shili Zhan , John N Brady
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摘要: Abstract Human insulin-like growth factor (IGF)-II mRNA has been shown to be expressed at high levels in a variety of tumors, including rhabdomyosarcomas. In addition, many tumors have alterations p53 expression. To investigate whether regulates IGF-II gene expression, we transfected wild-type expression vectors and luciferase constructs driven by P3 promoters into multiple cell lines. We found that reduced, dose-dependent manner, both endogenous transcripts The inhibition was more pronounced the two lines mutant protein, RD, HTB114. element responsible for this mapped minimal promoter region. also an HPV-16 E6 plasmid CCL13 cells containing functional up-regulated activity. Wildtype, but not mutant, interfered with binding TATA-binding protein TATA motif P3, although could directly associate human protein. Our results suggest may play role regulation
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