emerging role of the cerna-based malat-1-mirna network in polycystic ovary syndrome

Polycystic ovary syndrome (pcos) is a hormonal disorder and a common health problem that affects women at the early to late reproductive stage. several genetic and environmental factors such as obesity, liver diseases, imbalance of androgens, and menstrual dysfunction have contributed to the progression of pcos. research has shown a link between diabetes, hypertension, miscarriages, and cardiovascular disease with pcos. experimental discoveries have begun to evaluate the mechanisms involved in pcos. although various classical interventions are used in the treatment of pcos, current medications are not able to control outcomes of pcos and the management of this syndrome is still challenging. accumulating evidence showed that dysregulation of long non-coding rnas (lncrnas) is essential to pcos pathogenesis. lncrnas are a class of transcripts that mediate the process of gene expressions at the level of transcription and post-transcription. it has been found that lncrna metastasis‐associated lung adenocarcinoma transcript‐1 (malat1 or nuclear-enriched abundant transcript 2 (neat2)) presents a vital role in regulating pcos. malat-1 as a competing endogenous rna (cerna) can suppress micrornas (mirnas) and decrease granulosa cell proliferation, apoptosis, and pathogenesis. abnormal expression of malat1 is one of the prognostic factors for cell autophagy, migration, and drug resistance. malat1 can be used as a potential biomarker for treatment of pcos. however, the exact roles of malat1 in granulosa cells of women with pcos remain largely unknown and further studies are required to confirm its action. in the present article, we summarize the functions of the lncrna malat-1/mirna axes in women with pcos.