ArticleCell death discovery2024
LncRNA HOTAIR regulates autophagy and proliferation mechanisms in premature ovarian insufficiency through the miR-148b-3p/ATG14 axis.
Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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
15 citing papers in PubMed, 16 citations in OpenAlex.
- Bioengineering Ovarian Endocrine Function: From Follicle Modeling to Cell-Based Hormone Therapy.Advanced healthcare materials · 2026Review
- The degradation revolution: harnessing targeted protein degradation for the treatment of human diseases.Cellular and molecular life sciences : CMLS · 2026Review
- The ATG14: multi-layer autophagy control and an emerging therapeutic target in cancer.Apoptosis : an international journal on programmed cell death · 2026Review
- Crosstalk between microRNAs and autophagy in adipocyte differentiation: emerging therapeutic targets for obesity.Adipocyte · 2025Review
- The implications of LncRNAs and premature ovarian insufficiency.Journal of ovarian research · 2025Review
- Dysregulated lncRNAs in Cisplatin-Induced Nephrotoxicity and Their Association with Apoptosis and Autophagy: An Exploratory In Vitro Study.International journal of molecular sciences · 2025Article
- Autophagy in ovary: protective roles, pathological consequences, and unresolved issues.Journal of ovarian research · 2025Review
- The Role of Ovarian Granulosa Cells Related-ncRNAs in Ovarian Dysfunctions: Mechanism Research and Clinical Exploration.Reproductive sciences (Thousand Oaks, Calif.) · 2025Review
- Non-coding RNA-mediated granulosa cell dysfunction during ovarian aging: From mechanisms to potential interventions.Non-coding RNA research · 2025Review
- Long Non-Coding TP73-AS1: A Potential Biomarker and Therapeutic Target in Cancer.International journal of molecular sciences · 2025Review
- Chlorogenic Acid Ameliorates Chronic Unpredictable Stress-Induced Diminished Ovarian Reserve Through Ovarian Renin-Angiotensin System.Molecular nutrition & food research · 2025Article
- Non-hormone replacement therapy to overcome premature ovarian insufficiency: advances in natural products and stem cells targeting autophagy.Frontiers in endocrinology · 2025Review
- Exosomes Derived From Human Mesenchymal Stem Cells Mitigate Follicular Interstitial Cell Ferroptosis via the miR-26a-5p/PTEN/GPX4 Axis in Rats with Chemotherapy-Induced Premature Ovarian Insufficiency.International journal of nanomedicine · 2025Article
- Dysregulation of autophagy during photoaging reduce oxidative stress and inflammatory damage caused by UV.Frontiers in pharmacology · 2025Review
- Genetic insights into the complexity of premature ovarian insufficiency.Reproductive biology and endocrinology : RB&E · 2024Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Premature ovarian insufficiency (POI) is a serious disease significantly affecting the physical and mental health of women of reproductive age, not just impacting fertility outcomes. Ovarian damage due to chemotherapy remains a major cause of this condition. Recent studies have indicated the involvement of the long non-coding RNA HOTAIR in the progression of various diseases, showcasing important biological functions, yet its role in POI remains unclear. We conducted microarray dataset analysis and qRT-PCR experiments, demonstrating downregulation of HOTAIR expression in ovarian tissue and granulosa cells. Various functional experiments using plasmids overexpressing HOTAIR confirmed its promotion of cisplatin-induced granulosa cell autophagy and proliferation. Mechanistically, dual-luciferase assays showed that HOTAIR modulates ATG14 levels in POI by binding miR-148b-3p, thereby enhancing levels of autophagy and proliferation. In this study, we first explored the impact of miR-148b-3p on POI and found that overexpression of miR-148b-3p reversed the promotion of autophagy and proliferation induced by HOTAIR overexpression. The inhibitory effect of miR-148b-3p inhibitor on KGN cell autophagy and proliferation improvement could also be reversed by silencing ATG14. Overall, our findings indicate the promoting role of HOTAIR in POI and its potential as a biomarker for POI by modulating the miR-148b-3p/ATG14 axis to improve mechanisms of autophagy and proliferation in POI.
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.