Hypothesis: Androgen receptor/Aurora A kinase/NF-κB signaling axis induce inflammatory response during polycystic ovarian syndrome progression

Polycystic ovarian syndrome (PCOS) is one of the most frequent endocrinopathies, affecting women of reproductive age, and characterized by the presence of cysts, anovulation, hyperandrogenism, insulin resistance, and persistent inflammation. The prevalence rate of PCOS in India is comparatively high compared to other parts of the world, and it varies from 8 to 22% in reproductive age of women, whereas in other countries it ranges from 2 to 20%. However, the detailed molecular pathogenesis of PCOS is not fully understood. Studies on underlying molecular mechanism of PCOS will be necessary to understand the disease in detail and for delineating both therapeutic approaches and effective treatment regime. It was observed that androgens regulate the expression of Aurora A kinase in human cells, and several studies have reported that Aurora-A kinase up-regulates NF-κB signaling by phosphorylation of Ikappa Bα and induces inflammation in mice and humans during pathological conditions such as cancer. Based on this literature, we propose the hypothesis that a high clinical level of androgen, which is tightly associated to PCOS, binds to androgen receptors and subsequently increases Aurora A kinase expression, which may activate the NF-κB signaling pathway and induce inflammation and progression of PCOS. We also propose that Aurora A kinase inhibitors will be more effective in the treatment of PCOS.