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Updated: Aug 16, 2026

Production of Replication-Defective Retrovirus by Transient Transfection of 293T cells
Published on: December 4, 2007
Abrogation of IL-3 and IL-2 dependence by recombinant murine retroviruses expressing v-myc oncogenes
Abstract:
Several oncogenes are thought to cause transformation by affecting the signal transmission pathway of growth factors. One example is the induction of c-myc, the cellular homologue of the avian transforming oncogene v-myc, by platelet-derived growth factor (PDGF) among a set of genes associated with competence induction in fibroblasts. Another of the competence genes, r-fos, has been shown to be related to v-fos, the transforming gene of the FBJ sarcoma virus. In addition, PDGF induces c-fos, the cellular homologue of v-fos. The importance of c-myc induction is suggested by the observation that c-myc, under the control of a glucocorticoid regulator, can partially relieve the requirement of fibroblasts for PDGF. We have examined the effects of oncogenes on haematopoietic/lymphoid cell differentiation, immortalization and factor dependence for growth. Here we report the effects of recombinant murine retroviruses capable of expressing the avian v-myc. With interleukin-3 (IL-3)- or interleukin-2 (IL-2)-dependent cells, the viruses abrogated the requirement for growth factors and suppressed c-myc expression.
Insights
Avian v-myc oncogene expression abrogated growth factor dependence in hematopoietic cells. This oncogene suppressed c-myc expression, impacting cell growth regulation and differentiation.
Area of Science:
- Molecular Biology
- Oncology
- Cell Biology
Background:
- Oncogenes play a role in cell transformation by influencing growth factor signaling pathways.
- Platelet-derived growth factor (PDGF) induces c-myc and c-fos, genes associated with fibroblast competence.
- c-myc induction is critical, as its regulated expression can reduce fibroblast dependence on PDGF.
Purpose of the Study:
- To investigate the impact of oncogenes on hematopoietic and lymphoid cell differentiation, immortalization, and growth factor dependence.
- To examine the effects of avian v-myc oncogene expression in hematopoietic/lymphoid cells.
Main Methods:
- Utilized recombinant murine retroviruses to express the avian v-myc oncogene.
- Studied the effects on interleukin-3 (IL-3)-dependent and interleukin-2 (IL-2)-dependent cell lines.
Main Results:
- Recombinant avian v-myc expression abrogated the requirement for growth factors (IL-3 or IL-2) in dependent cell lines.
- v-myc expression led to the suppression of endogenous c-myc expression in these cells.
Conclusions:
- The avian v-myc oncogene can override the need for specific growth factors in hematopoietic/lymphoid cells.
- v-myc's ability to suppress c-myc suggests a complex regulatory role in cell proliferation and differentiation.
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