We investigated the biological significance of estrogen receptors (ERs) in NIH3T3 cell transformation by the [12Val] K-Ras mutant. This mutant enhanced the steady-level and transcriptional activity of ER. Coexpression of the progesterone receptor with mutant K-Ras led to suppression of tumorigenicity and inhibition of the activation of ER. The antisense oligomers complementary to the ER suppressed proliferation and transformed phenotypes of K12V cells. These observations support the importance of ER in Ras-mediated cell transformation.
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