Abstract
Polycystic ovary syndrome (PCOS) is one of the most common endocrinopathies and primarily presents with hyperandrogenism. Although environmental factors and genetic factors are thought to be the major reason, there still exists a lot of questions need to be answered. High expression of C‑terminal‑binding protein 1 antisense (CTBP1‑AS) was identified as an independent risk factor for PCOS; however, the molecular mechanism of CTBP1‑AS in PCOS regulation is unknown. In the present study, the expression level of CTBP1‑AS was found to be significantly upregulated in patients with PCOS compared with healthy control patients. CTBP1‑AS knockdown was demonstrated to reduce the proliferation and promote the apoptosis of granulosa tumor cells in vitro. It was also identified that the two core catalytic subunits of Polycomb repressive complex 2 (enhancer of zeste homolog 2 and embryonic and ectoderm development protein) interacted with CTBP1‑AS in primary granulosa cells and KGN cells. In addition, cryptotanshinone treatment was demonstrated to effectively downregulate CTBP1‑AS expression level. Data from the present study suggested a pathophysiological role of CTBP1‑AS in PCOS and may provide a new potential target for PCOS treatment.
Keywords:
C‑terminal‑binding protein 1 antisense; cryptotanshinone; embryonic ectoderm development protein; enhancer of zeste homolog 2; methylation; polycystic ovary syndrome.