Requirement of estrogen receptor expression and function for [12Val] K-Ras-mediated NIH3T3 cell transformation.
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.
Kato
K
K
Department of Reproductive Physiology and Endocrinology, Medical Institute of Bioregulation, Kyushu University, Beppu, Oita, Japan.
Sakamoto
T
T
Wake
N
N
D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D016889:Endometrial Neoplasms / Q000235:genetics* / Q000378:metabolism; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D009154:Mutation; D010641:Phenotype; D016283:Proto-Oncogene Proteins p21(ras) / Q000235:genetics* / Q000378:metabolism; D011960:Receptors, Estrogen / Q000235:genetics* / Q000378:metabolism; D011980:Receptors, Progesterone / Q000235:genetics; D014157:Transcription Factors; D014162:Transfection; D014407:Tumor Cells, Cultured; D014633:Valine
D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D014157:Transcription Factors; C501009:HRAS protein, human; D016283:Proto-Oncogene Proteins p21(ras); D014633:Valine