TI - Letrozole inhibits ER-alpha36 -mediated ERK and Akt PHOSphorylation . AB - Androgens are well-known to exert estrogenic effects via their aromatization to estrogens . Accumulating evidence suggest that estrogens are generated by in situ aromatization from cells of pathologically altered endometrium in postmenopausal women , which promotes malignant growth of these cells . Previous study also demonstrated that aromatase activity in the endometrium plays a vital role in the malignant transformation of endometrial cells by converting androgen into mitogenic estrogen in the endometrial tissue [24] . To determine the role of aromatase in non-genomic signaling pathway mediated by testosterone , we examined testosterone stimulated ERK and Akt PHOSphorylation in Hec1A cells pre-treated by letrozole , an aromatase inhibitor . As expected , letrozole abrogated the PHOSphorylation of ERK and Akt stimulated by testosterone ( Figure 4A and 4B ) . In addition , we also found that letrozole treatment reduced expression levels of aromatase in Hec1A cells (Figure 4C) . These data strongly suggest that aromatase is involved in testosterone activities in cells express ER-alpha36 .