Designer monotransregulators provide a basis for a transcriptional therapy for de novo endocrine-resistant breast cancer.

ABSTRACT: The main circulating estrogen hormone 17beta-estradiol (E2) contributes to the initiation and progression of breast cancer. Estrogen receptors (ERs), as transcription factors, mediate the effects of E2. Ablation of the circulating E2 and/or prevention of ER functions constitute approaches for ER-positive breast cancer treatments. These modalities are, however, ineffective in de novo endocrine-resistant breast neoplasms that do not express ERs. The interaction of E2-ERs with specific DNA sequences, estrogen responsive elements (EREs), of genes constitutes one genomic pathway necessary for cellular alterations. We herein tested the prediction that specific regulation of ERE-driven genes by an engineered monomeric and constitutively active transcription factor, monotransregulator, provides a

SUBMITTER: Nott SL 

PROVIDER: S-EPMC2781301 | biostudies-literature | 2010 Jan-Feb

REPOSITORIES: biostudies-literature