Thursday, June 28, 2012
Figure 1. SRC1
fragments on the endometriotic pathway. According to a study in Nature Medicine,
inhibition of a pathway that produces a fragment of nuclear receptor coactivator 1
(NCOA1; SRC1) in endometrial
(uterine lining) cells could help treat endometriosis.
menstruation, cells shed from the endometrium [a] can respond to local
increases in tumor necrosis factor-a (TNF-a) [b] by upregulating matrix metalloproteinase 9
which cleaves a 70 kDa, C-terminal fragment from full-length (160 kDa) SRC1 [d].
In turn, the fragment prevents TNF-a-induced
activation of procaspase-8 to caspase-8
[e(1)] and consequent apoptotic signaling, and it promotes the
epithelial-mesenchymal transition (EMT) [e(2)] by an unknown mechanism,
thereby inducing antiapoptotic and invasive phenotypes, respectively. These
characteristics are the hallmarks of endometriotic cells [f] and enable
them to form endometriotic lesions [g] on the ovaries and/or elsewhere
in the peritoneum.