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Updated: Aug 14, 2026
Transduction-Transplantation Mouse Model of Myeloproliferative Neoplasm
Published on: December 22, 2016
Transfected mouse c-jun can inhibit transformation of primary rat embryo fibroblasts
D Ginsberg1, S I Hirai, O Pinhasi-Kimhi
1Department of Chemical Immunology, Weizmann Institute of Science, Rehovot, Israel.
Abstract:
The c-jun gene, which encodes a transcriptional regulatory protein, is the cellular homologue of the transforming gene of avian sarcoma virus 17. In an attempt to assess the biological activities of mouse c-jun, we studied the consequences of its overproduction in an in vitro transformation assay. A c-jun expression plasmid failed to cooperate with either ras, myc or mutant p53 in this focus formation assay. On the other hand, it dramatically inhibited the ability of various oncogene combinations to elicit foci upon transfection into primary rat embryo fibroblasts. Deletion plasmids lacking either the transactivating domain or the leucine repeat of c-jun still displayed a pronounced inhibitory activity. On the contrary, a plasmid encoding only the first 187 amino acids of c-jun had no such activity. The data suggests that enhanced c-jun expression may interfere with the induction or proliferation of transformed cells in this system, and that the inhibitory activity resides in the C-terminal half of the molecule.
Insights
Overexpressing the c-jun gene, a key regulator, surprisingly inhibited cell transformation in experiments. This suggests enhanced c-jun activity may block cancer cell development, with the effect localized to the protein's C-terminal region.
Area of Science:
- Molecular Biology
- Oncology
- Gene Regulation
Background:
- The c-jun gene encodes a transcriptional regulatory protein and is homologous to a viral transforming gene.
- Understanding the biological activities of c-jun is crucial for cancer research.
Purpose of the Study:
- To investigate the effects of mouse c-jun overproduction on cell transformation in vitro.
- To identify the specific regions of c-jun responsible for its biological activity.
Main Methods:
- Utilized an in vitro transformation assay using primary rat embryo fibroblasts.
- Employed c-jun expression plasmids and deletion mutants to assess focus formation.
- Co-transfected cells with oncogenes (ras, myc, mutant p53) and c-jun constructs.
Main Results:
- Overproduction of c-jun did not cooperate with oncogenes like ras, myc, or mutant p53 in transformation.
- Enhanced c-jun expression significantly inhibited focus formation induced by oncogene combinations.
- Deletion analysis revealed that the C-terminal half of c-jun, excluding the N-terminal 187 amino acids, mediates this inhibitory activity.
Conclusions:
- Enhanced c-jun expression can interfere with the induction and proliferation of transformed cells.
- The inhibitory function of c-jun in this system is primarily located in its C-terminal region, specifically involving the transactivating domain and leucine repeat.
