The role that a particular steroid receptor coactivator, SRC-1, plays in the progression of endometriosis is elucidated in a paper published online in Nature Medicine this week. The work suggests that this protein could be used as a molecular target for the therapy of this disease.
Endometriosis is considered to be an estrogen-dependent inflammatory disease of the uterus. Previously, Bert W O’Malley and colleagues found lowered amounts of the full length SRC-1 protein in endometriotic tissue but how it contributes to disease progression remains unknown.
The authors now find that a previously unidentified truncated form of the protein, 70-kDa SRC-1, is highly elevated both in the endometriotic tissue of mice with surgically induced endometriosis and in endometriotic cells of the microenvironment of tissue samples from individuals with the disease. This increase is caused in response to signalling from the inflammatory mediator TNF-alpha.
The authors therefore propose a new pathogenic pathway, involving a shorter form of SRC-1, for the progression of endometriosis. The finding also suggests that the TNF-alpha therapy, etanercept, may be useful to treat this disease.