What is it about?
Many estrogen receptor-positive (ER+) breast tumors become estrogen receptor-negative (ER-) after receiving hormone therapy, thus developing resistance to the treatment. The reasons for this transformation have been unclear. We discovered that when breast cancer cells don't get enough of an amino acid called serine, they change how they use sugar for energy and also how they read certain genes. This change affects a key pathway in the cell related to estrogen, a hormone. When cells are low on serine, they can't properly use sugar to produce a molecule called acetyl-CoA, which helps activate certain genes. One of the major genes affected controls the estrogen response in the cell. Without enough of this gene being read and activated, the breast cancer cells act as if they don't respond to estrogen, which can make the cancer harder to treat.
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Why is it important?
Once we understand how estrogen receptor-positive (ER+) breast tumors become estrogen receptor-negative (ER-) , we will be able to develop therapeutic methods to prevent this transition and hormone resistance.
Read the Original
This page is a summary of: Serine starvation silences estrogen receptor signaling through histone hypoacetylation, Proceedings of the National Academy of Sciences, September 2023, Proceedings of the National Academy of Sciences, DOI: 10.1073/pnas.2302489120.
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