Title : Repression of ESR1 transcription by MYOD potentiates letrozole-resistance in ERα-positive breast cancer cells.

Pub. Date : 2017 Oct 21

PMID : 28842253






6 Functional Relationships(s)
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Compound Name
Protein Name
Organism
1 Repression of ESR1 transcription by MYOD potentiates letrozole-resistance in ERalpha-positive breast cancer cells. Letrozole estrogen receptor 1 Homo sapiens
2 Repression of ESR1 transcription by MYOD potentiates letrozole-resistance in ERalpha-positive breast cancer cells. Letrozole estrogen receptor 1 Homo sapiens
3 Transcriptional silencing of estrogen receptor alpha (ERalpha) expression is an important etiology contributing to the letrozole-resistance in ERalpha-positive breast cancer (BCa) cells, but the transcription factors responsible for this transcriptional repression remain largely unidentified. Letrozole estrogen receptor 1 Homo sapiens
4 Transcriptional silencing of estrogen receptor alpha (ERalpha) expression is an important etiology contributing to the letrozole-resistance in ERalpha-positive breast cancer (BCa) cells, but the transcription factors responsible for this transcriptional repression remain largely unidentified. Letrozole estrogen receptor 1 Homo sapiens
5 Transcriptional silencing of estrogen receptor alpha (ERalpha) expression is an important etiology contributing to the letrozole-resistance in ERalpha-positive breast cancer (BCa) cells, but the transcription factors responsible for this transcriptional repression remain largely unidentified. Letrozole estrogen receptor 1 Homo sapiens
6 Mechanistically, MYOD was shown to be a potent corepressor of ESR1 transcription, and this transcriptional repression was significantly enhanced in the presence of letrozole treatment. Letrozole estrogen receptor 1 Homo sapiens