Related Experiment Video
Updated: Feb 4, 2026

Author Spotlight: Investigating the Mechanisms and Inducing Models of Polycystic Ovary Syndrome
Published on: July 5, 2024
Long non-coding RNA LINC-01572:28 inhibits granulosa cell growth via a decrease in p27 (Kip1) degradation in patients
Jun Zhao1, Jieying Xu1, Wangshen Wang1
1Center for Reproductive Medicine, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200135, China; Shanghai Key Laboratory for Assisted Reproduction and Reproductive Genetics, Shanghai 200135, China.
Background:
Disordered folliculogenesis is a key feature of polycystic ovary syndrome (PCOS), but the underlying molecular mechanism remains unclear.
Methods:
Long non-coding RNA (lncRNA) expression in luteinized granulosa cells (hLGCs) derived from women with and without PCOS were analyzed using microarray and qRT-PCR. Immortalized human granulosa cell lines were cultured for proliferation assays after transfection with the LINC-01572:28 over-expression vector in the presence or absence of p27 siRNA. Protein expression analysis, rescue assays, and RNA immunoprecipitation (RIP) were used to confirm the LINC-01572:28 substrate.
Findings:
LINC-01572:28 and p27 protein were elevated whereas proliferating cell nuclear antigen protein was decreased in the hLGCs of women with PCOS. LINC-01572:28 expression was positively correlated with basal testosterone levels. Over-expression of LINC-01572:28 inhibited cell proliferation and impeded G1/S transition, which were partially reversed by siRNA-mediated p27 knockdown.
Interpretation:
Our findings, therefore, suggest that LINC-01572:28 suppresses cell proliferation and cell cycle progression by reducing the degradation of p27 protein via SKP2 binding.
Insights
Polycystic ovary syndrome (PCOS) involves disordered folliculogenesis. This study found that LINC-01572:28, elevated in PCOS, inhibits granulosa cell proliferation by stabilizing p27 protein.
Area of Science:
- Reproductive biology
- Molecular endocrinology
- Genetics
Background:
- Polycystic ovary syndrome (PCOS) is characterized by disordered folliculogenesis, with unclear molecular mechanisms.
- Granulosa cell dysfunction is implicated in PCOS pathogenesis.
Purpose of the Study:
- To investigate the role of long non-coding RNA (lncRNA) LINC-01572:28 in PCOS-related disordered folliculogenesis.
- To elucidate the molecular mechanism by which LINC-01572:28 affects granulosa cell function.
Main Methods:
- Microarray and qRT-PCR analysis of lncRNA expression in human luteinized granulosa cells (hLGCs) from women with and without PCOS.
- Cell proliferation assays, Western blotting, and RNA immunoprecipitation (RIP) in immortalized granulosa cell lines.
- Manipulation of LINC-01572:28 and p27 expression using overexpression vectors and siRNA.
Main Results:
- LINC-01572:28 and p27 protein levels were elevated in hLGCs from women with PCOS.
- Overexpression of LINC-01572:28 inhibited hLGC proliferation and G1/S cell cycle transition.
- LINC-01572:28 overexpression led to decreased degradation of p27 protein, partially reversed by p27 knockdown.
Conclusions:
- LINC-01572:28 plays a significant role in suppressing granulosa cell proliferation and cell cycle progression in PCOS.
- The mechanism involves LINC-01572:28 reducing p27 protein degradation through binding to SKP2.
- LINC-01572:28 represents a potential therapeutic target for PCOS.
Related Concept Videos
Proteins: From Genes to Degradation
Transcription is the synthesis of RNA...
lncRNA - Long Non-coding RNAs
Decreasing Function
Regulated Protein Degradation
Protein degradation plays two important roles in the cells. It helps to protect cells from misfolded or damaged proteins before they lead to a...
Ovaries
On the ovarian surface, a layer of...
Feedback Inhibition

