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Significance Many estrogen receptor–positive (ER+) breast cancers lose ER expression and become resistant to endocrine therapy and progress. Unfortunately, the molecular mechanisms underlying the loss of ER expression in breast… Click to show full abstract
Significance Many estrogen receptor–positive (ER+) breast cancers lose ER expression and become resistant to endocrine therapy and progress. Unfortunately, the molecular mechanisms underlying the loss of ER expression in breast cancer are poorly understood. This study identifies 14-3-3τ as a key driver of ER loss. We further elucidate a regulation of ERα36 by 14-3-3τ-GATA3 interaction as the mechanism of 14-3-3τ-driven ER loss in breast cancer. The in vitro tumor spheroid model established in our study mimics the evolution of ER+ to ER– human breast cancer and provides a very useful model for future investigation.
Journal Title: Proceedings of the National Academy of Sciences of the United States of America
Year Published: 2022
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