Open AccessCTBP1‑AS upregulation is associated with polycystic ovary syndrome and can be effectively downregulated by cryptotanshinone
Author(s) -
Mingxiao Wen,
Xiaoqing Dou,
Shuzhen Zhang,
Bin Wang,
Jiangyan Xu,
Wenchao Zhang,
Feifei Wang
Publication year - 2022
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2022.12761
Subject(s) - downregulation and upregulation , polycystic ovary , oncogene , molecular medicine , cell cycle , cancer research , ovary , biology , apoptosis , microbiology and biotechnology , medicine , endocrinology , gene , genetics , insulin resistance , insulin
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.