ArticleHeliyon2024
LncRNA PKD1P6 modulates ovarian granulosa cell survival of hyperandrogenic polycystic ovary syndrome by targeting miR-135b-5p and inhibiting ERK1/2 signaling.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Roles of exosomes in microenvironment-related premature ovarian insufficiency: mechanisms and therapeutic intervention.Reproductive biology and endocrinology : RB&E · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polycystic ovary syndrome (PCOS) is the most common and multifactorial endocrine disease among women of reproductive age. Aberrant folliculogenesis is a common pathological characteristic of PCOS, but the underlying molecular mechanism remains unclear. Emerging evidence indicated that aberrant expression of long noncoding RNAs (lncRNAs) may contribute to the pathogenesis of PCOS. In this study, we found that lncRNA PKD1P6 expression was remarkably down-regulated in ovarian granulosa cells (GCs) of hyperandrogenic PCOS (HA-PCOS) patients and negatively correlated with serum testosterone (T) levels. We further showed that overexpression of PKD1P6 markedly reduced cell viability, attenuated DNA synthesis capacity, arrested the cell cycle at G0/G1 phase and promoted apoptosis of KGN cells. Exosomes derived from PKD1P6 overexpression cells exerted similar effects to PKD1P6 overexpression on the function of KGN cells. Mechanistically, PKD1P6 could act as a competing endogenous RNA (ceRNA) by directly binding with miR-135b-5p. Overexpression of PKD1P6 significantly suppressed ERK1/2 activation, whereas up-regulation of miR-135b-5p exerted an opposing effect. Additionally, excessive androgen was showed to diminish PKD1P6 expression while promote miR-135b-5p expression of PCOS models in vitro and vivo. Collectively, our findings delineate the clinical significance of PKD1P6 in HA-PCOS and the new regulatory mechanisms involved in abnormal folliculogenesis, providing a promising therapeutic target for HA-PCOS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.