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Activation of the transforming potential of a normal cell sequence: a molecular model for oncogenesis
Abstract:
The molecularly cloned, long terminal repeat (LTR) of the Moloney sarcoma virus (M-MSV) provirus has been covalently linked to c-mos, the cellular homolog of the M-MSV-specific sequence, v-mos. These newly constructed clones lack any M-MSV-derived sequences other than the LTR, but in DNA transfection assays they transform cells as efficiently as cloned subgenomic M-MSV fragments containing both v-mos and LTR. Cells transformed by LTR:c-mos hybrid molecules contain additional copies of mos DNA, and several size classes of polyadenylated RNA's with sequence homology to mos. The activation of the transforming potential of c-mos by the proviral LTR suggests a model whereby LTR-like elements could activate other normal cell sequences with oncogenic potential.
Insights
The long terminal repeat (LTR) from Moloney sarcoma virus activates cellular mos (c-mos) oncogenes. This finding suggests LTR-like elements can activate other cellular genes, potentially leading to cancer.
Area of Science:
- Molecular biology
- Virology
- Oncogenesis
Background:
- The Moloney sarcoma virus (M-MSV) contains a viral oncogene, v-mos.
- Cellular homologs of viral oncogenes (cellular proto-oncogenes) are implicated in cancer.
- Understanding how viral elements activate cellular genes is crucial for cancer research.
Purpose of the Study:
- To investigate the transforming potential of the cellular mos gene (c-mos).
- To determine if the long terminal repeat (LTR) of M-MSV can activate c-mos.
- To explore the mechanism of oncogene activation by viral LTRs.
Main Methods:
- Molecular cloning of viral and cellular gene sequences.
- Construction of hybrid DNA molecules linking M-MSV LTR to c-mos.
- DNA transfection assays to assess cellular transformation.
- Analysis of gene expression using RNA hybridization.
Main Results:
- LTR:c-mos hybrid molecules efficiently transformed cells, similar to M-MSV fragments.
- Transformed cells showed increased copies of mos DNA and mos-homologous RNAs.
- The viral LTR activated the oncogenic potential of the cellular c-mos gene.
Conclusions:
- Viral LTRs can activate the transforming ability of cellular proto-oncogenes like c-mos.
- This activation mechanism provides a model for how LTR-like elements may contribute to oncogenesis.
- Further research into LTR-mediated proto-oncogene activation is warranted.