RETRACTED ARTICLE: Long non-coding RNA placenta‑specific protein 2 regulates micorRNA-19a/tumor necrosis factor α to participate in polycystic ovary syndrome

Abstract

Polycystic ovary syndrome (PCOS) is a type of hormonal disorder that affects about 5–20% of females at their reproductive age worldwide. MicorRNA-19a (miR-19a) is a well-characterized miRNA in cancer biology and its function is mainly mediated by targeting tumor necrosis factor α (TNF-α), which plays critical roles in PCOS. Our preliminary analysis predicted the potential interaction between miR-19a 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-19a. qPCR assays were performed for the expression analysis of miR-19a/TNF-α. In addition, Western blot analysis and cell apoptosis assay were conducted. The results showed that PLAC2 was upregulated in PCOS. PLAC2 and miR-19a showed a direct interaction, while overexpression of PLAC2 and miR-19a did not affect the expression of each other in KGN cells. Instead, overexpression of PLAC2 led to upregulated TNF-α, which is a target of miR-19a. Cell apoptosis analysis showed that PLAC2 and TNF-α 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-19a. Therefore, PLAC2 may regulate miR-19a/TNF-α to participate in PCOS.

Whispers of the polycystic ovary syndrome theater: Directing role of long noncoding RNAs

“…A direct interaction between lncRNA placenta-specific protein 2 and miR-19a has been identified. Overexpression of placenta-specific protein 2 in KGN cells led to upregulated tumor necrosis factor-α, which is also a target of miR-19a, which subsequently promoted KGN cell apoptosis [ 31 ]. In addition, through competitive binding with miR-130a, lncRNA HOX transcript antisense RNA (HOTAIR) increased insulin-like growth factor-1 expression and GC apoptosis, aggravating endocrine disorders in PCOS rat models [ 32 ].…”

“…PLAC2 and TNF-α promoted the apoptosis of GCs. [ 31 ] Human GCs and follicular fluid PVT1 (plasmacytoma Variant Translocation 1) Up Inhibited lncRNA PVT1 and overexpressed miR-17-5p result in downregulation of PTEN and promotion of cell proliferation, as well as inhibition of apoptosis of ovarian granulosa cells in PCOS. [ 35 ] Human cumulus cells KGN cells PWRN2 (Prader-Willi region nonprotein coding RNA 2) Up PWNR2 plays important roles in oocyte nuclear maturation in PCOS by functioning as a ceRNA to reduce the availability of miR-92b-3p for TMEM120B target binding during oocyte maturation in PCOS.…”

Modulation of the Inflammatory Response in Polycystic Ovary Syndrome (PCOS)—Searching for Epigenetic Factors

“…Continuing the topic of ncRNAs, an interaction between miR-19a and long ncRNA (lncRNA) placenta-specific protein 2 (PLAC2) may be crucial for the regulation of TNF-α signaling and consequently the activation of the transcription factor NF-κB and apoptosis in ovarian GCs [ 129 ]. As a multifunctional cytokine and adipokine, TNF-α exerts pleiotropic effects on many cell types and tissues, including ovarian and adipose tissues of PCOS patients [ 130 ].…”