Molecular Cell paper suggests that this action increases the life of estrogen molecules and may block BRCA1’s restrictive effects.
Methylation of estrogen receptors prolongs the life of these growth-driving molecules in breast cancer cells, according to scientists at Emory University’s Winship Cancer Institute.
The investigators found that an enzyme called SET7 methylates a flexible part of the estrogen receptor. When they created breast cancer cells with reduced levels of SET7, the estrogen receptor molecules lasted only half as long and were less effective in turning on genes.
The methylation appears in exactly the same spot where the tumor suppressor BRCA1 adds a different kind of regulatory marking and may block BRCA1’s restrictive effects on the estrogen receptor. The team also showed that a mutation in the estrogen receptor found in more aggressive breast tumors interferes with this methylation.
The results will be published in the May 9 issue of Molecular Cell.