Long non-coding RNA placenta-specific protein 2 regulates micorRNA-19a/tumor necrosis factor α to participate in polycystic ovary syndrome

Polycystic ovary syndrome (PCOS) is a type of hormonal disorder that affects about 5-20% of females at their reproductive age worldwide. MicorRNA-19 alpha (miR-19 alpha) is a well-characterized miRNA in cancer biology and its function is mainly mediated by targeting tumor necrosis factor alpha (TNF-alpha), which plays critical roles in PCOS. Our preliminary analysis predicted the potential interaction between miR-19 alpha and long non-coding RNA (lncRNA) placenta-specific protein 2 (PLAC2). Therefore, this study aimed to explore the role of PLAC2 in PCOS. Ovarian tissues were collected from 62 PCOS patients and 62 healthy females. Granulosa-like tumor cells (KGN) was prepared, and transient transfections was conducted. Dual-luciferase activity assay was used to investigate the interaction between PLAC2 and miR-19 alpha. qPCR assays were performed for the expression analysis of miR-19 alpha/TNF-alpha. In addition, Western blot analysis and cell apoptosis assay were conducted. The results showed that PLAC2 was upregulated in PCOS. PLAC2 and miR-19 alpha showed a direct interaction, while overexpression of PLAC2 and miR-19 alpha did not affect the expression of each other in KGN cells. Instead, overexpression of PLAC2 led to upregulated TNF alpha, which is a target of miR-19 alpha. Cell apoptosis analysis showed that PLAC2 and TNF-alpha promoted the apoptosis of KGN cells. Overexpression of miR-19a played an opposite role. In addition, the overexpression of PLAC2 reduced the effects of overexpression of miR-19 alpha. Therefore, PLAC2 may regulate miR-19 alpha/TNF-alpha to participate in PCOS.

Automated summary

This study reveals that PLAC2 may participate in PCOS by regulating the miR-19 alpha/TNF-alpha signaling pathway, which is of great significance for understanding the pathogenesis of PCOS.