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Updated: Aug 5, 2026

Comparative Lesions Analysis Through a Targeted Sequencing Approach
Published on: November 5, 2019
Characterization of changes in gene expression associated with malignant transformation by the NF-kappaB family
O Petrenko1, I Ischenko, P J Enrietto
1Department of Microbiology, State University of New York at Stony Brook, 11794, USA.
Abstract:
In this study, alterations in gene expression patterns have been examined in v-Rel-transformed avian bone marrow cells. Using a conditional v-Rel estrogen receptor chimera (v-RelER) which transforms cells in an estrogen-dependent manner, we constructed subtraction cDNA libraries from v-RelER-transformed bone marrow cells. Several different sequences were identified whose expression was altered upon hormone activation of v-RelER. These include two genes related to the MIP-1 chemokine family (mip-1beta and a tca3 homologue), a cell surface antigen sca-2 and the transcription factor nfkb1. The expression of each gene was assayed in a number of wild-type and mutant v-Rel-expressing fibroblast and hematopoietic cells. All v-Rel-transformed hematopoietic cells tested express high levels of nfkb1 and sca-2. In fibroblasts, wild-type v-Rel induced expression of mip-1beta and nfkb1, while nontransforming mutants of v-Rel failed to do so, suggesting a role for these two genes in v-Rel mediated transformation. Finally, these genes are expressed at high levels in cells overexpressing wild-type and truncated forms of c-Rel, implying that v-Rel transforms, in part, by induction of c-Rel target genes.
Insights
Avian bone marrow cells transformed by v-Rel show altered gene expression. This study identifies key genes like MIP-1 chemokines and NF-kB1 involved in v-Rel mediated transformation.
Area of Science:
- Molecular Biology
- Oncology
- Immunology
Background:
- v-Rel is a viral oncogene that transforms cells.
- Understanding gene expression changes is crucial for cancer research.
Purpose of the Study:
- To identify genes whose expression is altered by v-Rel transformation.
- To investigate the role of these genes in v-Rel mediated oncogenesis.
Main Methods:
- Conditional v-Rel estrogen receptor chimera (v-RelER) for estrogen-dependent transformation.
- Subtraction cDNA library construction to identify differentially expressed genes.
- Gene expression analysis in various cell types (fibroblasts, hematopoietic cells).
Main Results:
- Identified altered expression of MIP-1 chemokine family genes (mip-1beta, tca3 homologue), sca-2 antigen, and NF-kB1 transcription factor.
- v-Rel transformation upregulated NF-kB1 and sca-2 in hematopoietic cells.
- Wild-type v-Rel induced mip-1beta and NF-kB1 in fibroblasts, unlike non-transforming mutants.
- These genes are also upregulated by c-Rel overexpression, suggesting a shared pathway.
Conclusions:
- v-Rel transforms cells, in part, by inducing target genes of c-Rel.
- NF-kB1 and MIP-1beta are implicated in v-Rel mediated transformation.
- Gene expression profiling provides insights into viral oncogenesis mechanisms.
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