Xu G, Gai Q, James C B
Department of Biological Sciences, Program in Molecular and Cellular Biology, Ohio University, Athens 45701, USA.
Cancer Lett. 1998 Jan 30;123(2):199-205. doi: 10.1016/s0304-3835(97)00425-4.
The c-myc promoter has a unique characteristic showing both RNA polymerase II (pol II) and RNA polymerase III (pol III) activities. Previous studies demonstrated that activating PKC results in upregulation of c-myc expression from its pol II promoter. However, how PKC activation affects expression from the pol III promoter of the c-myc gene is not well understood. This study examines the effect of PKC on the pol III transcription from the c-myc gene by using an in vitro system. We report the inhibition of the c-myc pol III transcript by activating PKC. Further, either a phosphocellulose fraction of HeLa whole cell extract (WCE) enriched for transcription factor TF IIIB, or recombinant TATA-box binding protein could restore the inhibited c-myc pol III transcription under conditions that activate PKC. A role has been proposed for the c-myc pol III transcript in the regulation of c-myc gene expression. Therefore, this report discusses the significance of the downregulation of c-myc expression from its pol III promoter and the possible interplay between the pol II and pol III promoters of this gene.