We have demonstrated CYP17 mRNA and protein expression and activity in human trophoblasts. Considering the precursor concentration, blood flow, and mass of the placenta, we suggest that its contribution of androgens is an important source of estrogen production in pregnancy.

These results suggest that the AP-1 transcription factor, c-fos, may be one of the factors responsible for CYP17 repression and hence suppression of androstenedione production in granulosa cells. This may provide an explanation for the lack of CYP17 in granulosa cells.

Traditionally, in women, only the theca cells in the ovary and the zona reticularis layer of the adrenal cortex are believed to synthesize androgens. Interestingly, their neighboring cell layers, the granulosa cells and the zona glomerulosa cells, respectively, do not produce androgens. Recent literature has highlighted the role of the activator protein (AP-1) transcription factor, c-Fos, in the dynamics of this structural and functional relationship. Differential expression of c-Fos is believed to result in distinct patterns of steroidogenesis among these compartments in both the ovary and the adrenal glands. Clinically, deficient c-Fos levels have been implicated in the pathogenesis of polycystic ovary syndrome (PCOS). In this review, we discuss the pivotal role of c-Fos in controlling the expression of CYP17 and hence androgen production in various organ systems throughout the human body.

Background: Our previous work demonstrated that the human placenta expresses CYP17 and is capable of de novo production of C-19 steroids; thus, it has intrinsic capacity to generate estrogens without fetal or maternal steroid precursors.

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