Display options
Share it on

Int J Oncol. 1995 Sep;7(3):453-9. doi: 10.3892/ijo.7.3.453.

Suppression and restoration of v-SRC expression in rsv transformed-cells after transfection with N-ras and its antagonist.

International journal of oncology

E Tchevkina, N Kisseljova, M Shtutman, E Musatkina, O Mizenina, K Leskov, A Tavitian, F Kisseljov

Affiliations

  1. CTR CANC RES,INST CARCINOGENESIS,MOSCOW,RUSSIA. INSERM,U248,F-75010 PARIS,FRANCE.

PMID: 21552859 DOI: 10.3892/ijo.7.3.453

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.

Publication Types