Two serum response elements mediate transcriptional repression of human smooth muscle alpha-actin promoter in ras-transformed cells.

Bushel P, Kim JH, Chang W, Catino JJ, Ruley HE, Kumar CC
Oncogene. 1995 10 (7): 1361-70

PMID: 7731687

The mechanism by which activated ras oncogene expression leads to repression of genes encoding specific actin filament proteins is not understood. However, these changes associated with loss of organized actin filaments, are necessary to maintain the transformed phenotype. The human smooth muscle (sm) alpha-actin promoter is repressed in ras-transformed fibroblast cells and derepressed in revertant cell lines. In this study, we demonstrate that two serum response elements (SREs) present in the alpha-actin promoter are required for transcriptional repression in ras-transformed cells and the two SREs act synergistically to repress heterologous promoters in a ras-transformation dependent manner. Serum response factor (SRF), which can bind to the sm alpha-actin SREs, restores alpha-actin promoter activity in ras-transformed cells. c-Fos, c-Jun and YY1 also repress alpha-actin promoter through SREs, suggesting that these transcription factors may play a role in repressing alpha-actin promoter in ras-transformed cells.

MeSH Terms (17)

Actins Base Sequence Cell Transformation, Neoplastic DNA-Binding Proteins DNA Primers Gene Expression Regulation, Neoplastic Genes, ras Humans Molecular Sequence Data Muscle, Smooth Nuclear Proteins Promoter Regions, Genetic Repressor Proteins RNA, Messenger Sequence Deletion Serum Response Factor Transcription, Genetic

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