Several genes are induced constitutively in cells transformed by the v-src oncoprotein. This induction is generally dependent on the activation of transcription factors binding to src-responsive elements of the promoter. In previous studies, we showed that the induction of the CEF-4/9E3 cytokine gene by pp60(v-src) is dependent on the PRDII/κB domain of the promoter. In this investigation, we describe the activation of the HIV-1 LTR by pp60(v-src) and show that a region of 30 bp containing the two NF-KB binding sites is critical for activation of the promoter. The induction was dependent on transformation since non-transforming forms of pp60(v-src) had little or no effect on the promoter. The expression of proviral DNA and the release of p24 antigen were also increased by v-src indicating that viral replication was stimulated in src-transformed cells. The effect of v-src on HIV-1 gene expression occurred in the presence or in the absence of the tat viral trans-activator, in fibroblasts and in Jurkat T lymphocytes. These results indicate that several promoters controlled by PRDII/κB may be activated constitutively in v-src transformed cells and suggest that oncogenic tyrosine kinases may play a role in the induction of viruses with a PRDII/κB-controlled promoter.
|Number of pages||5|
|Publication status||Published - 1 Aug 1994|
ASJC Scopus subject areas
- Molecular Biology
- Cancer Research