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Updated: Jun 2, 2026
Generation, Amplification, and Titration of Recombinant Respiratory Syncytial Viruses
Published on: April 4, 2019
Suppression and restoration of v-SRC expression in rsv transformed-cells after transfection with N-ras and its
E Tchevkina1, N Kisseljova, M Shtutman
1CTR CANC RES,INST CARCINOGENESIS,MOSCOW,RUSSIA. INSERM,U248,F-75010 PARIS,FRANCE.
Abstract:
Previously, it was shown that hamster cells transformed by Rous Sarcoma Virus (RSV) exhibited a decreased expression of the RSV products (including the pp60 src oncogene) when these cells were supertransfected with the N-ras oncogene. To assess the responsibility of the activated N-ras in the modulation of the RSV viral products, a strategy based on two ras antagonists was used; i.e. i) a rap1A/K-rev1 expression vector known for its capacity to revert the K-ras induced transformed phenotype and ii) a plasmid containing antisense N-ras sequence. We present data showing only the plasmid construct containing the N-ras antisense sequense could inhibit expression or N-ras and, at the same time, restore the expression of v-src, up to a level comparable to that of the parental cells. Our results support the idea that some biological switches, triggered and activated through the N-ras oncogene pathway, might modulate the promoter activity of the RSV LTR.
Insights
The N-ras oncogene suppresses Rous Sarcoma Virus (RSV) products, including v-src. Inhibiting N-ras with an antisense sequence restored v-src expression, suggesting N-ras modulates RSV LTR activity.
Area of Science:
- Molecular Biology
- Oncology
- Virology
Background:
- Rous Sarcoma Virus (RSV)-transformed hamster cells show reduced RSV product expression when transfected with the N-ras oncogene.
- The N-ras oncogene's role in modulating RSV products requires further investigation.
Purpose of the Study:
- To determine if the activated N-ras oncogene is responsible for the decreased expression of RSV products.
- To investigate the mechanism by which N-ras influences RSV LTR promoter activity.
Main Methods:
- Utilized two ras antagonists: a rap1A/K-rev1 expression vector and a plasmid with an antisense N-ras sequence.
- Assessed the impact of these antagonists on N-ras and v-src expression in RSV-transformed hamster cells.
Main Results:
- Only the antisense N-ras sequence effectively inhibited N-ras expression.
- Inhibition of N-ras expression restored v-src expression to levels comparable to parental cells.
- The rap1A/K-rev1 vector did not significantly alter N-ras or v-src expression.
Conclusions:
- The N-ras oncogene pathway plays a crucial role in downregulating RSV viral products.
- N-ras likely modulates the promoter activity of the RSV Long Terminal Repeat (LTR) through specific biological switches.
