ArticleScientific reports2024
ER stress-induced LINC00173 promotes the apoptosis of ovarian granulosa cells by regulating the HRK/PI3K/AKT pathway in polycystic ovary syndrome.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Molecular Mechanisms Underlying Reproductive Dysfunction in Polycystic Ovary Syndrome.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Identification and validation of an endoplasmic reticulum stress related model to predict prognosis and tumor microenvironment in neuroblastoma.BMC cancer · 2026Article
- Network pharmacology and molecular docking reveal the mechanism of Zishen Yutai Wan against polycystic ovary syndrome.Journal of ovarian research · 2026Article
- BRCA1 alleviates inflammation, oxidative stress, and ovarian granulosa cell apoptosis by inhibiting endoplasmic reticulum stress, thereby ameliorating polycystic ovary syndrome.European journal of medical research · 2026Article
- Pathogenesis and treatment of obesity-related polycystic ovary syndrome.Journal of ovarian research · 2025Review
- Review
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Authors and funding
8 authors.
Funding
Abstract
Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder and metabolic abnormality disease that mainly affects women of reproductive age. LINC00173, a novel long noncoding RNA (lncRNA), has emerged as an important factor in the development of PCOS. However, the role of LINC00173 in PCOS development and its specific upstream and downstream mechanisms remain to be further clarified. Here, we found that LINC00173 was significantly upregulated in granulosa cells (GCs) of PCOS patients, and played a crucial role in promoting apoptosis of GCs. Mechanistically, we observed the activation of endoplasmic reticulum (ER) stress in the GCs of PCOS patients, and the ER stress sensor ATF4 could directly induce LINC00173 expression by binding to its promoter. LINC00173 further upregulated the expression of Harakiri (HRK) and subsequently inhibited downstream PI3K/AKT pathway. In conclusions, our study uncovered that ER stress-induced upregulation of LINC00173 leads to increased HRK expression and inhibition of the PI3K/AKT pathway, thereby promoting the progression of PCOS. These findings provide a new therapeutic strategy for the treatment of PCOS.
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