ArticleEndocrinology2014
Inactivation of AKT induces cellular senescence in uterine leiomyoma.
Article in Endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- A Systematic Review of the Role of Senescent Cells in Uterine Leiomyomas: Deciphering Molecular Pathways and Exploring Therapeutic Prospects.Reproductive sciences (Thousand Oaks, Calif.) · 2026Pooled it
- Article
- UTERINE FIBROIDS.Physiological reviews · 2025Review
- Nanosize Non-Viral Gene Therapy Reverses Senescence Reprograming Driven by PBRM1 Deficiency to Suppress iCCA Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Senescence-associated secretory phenotype (SASP) and uterine fibroids: Association with PD-L1 activation and collagen deposition.Ageing research reviews · 2024Review
- Modulation of tumor plasticity by senescent cells: Deciphering basic mechanisms and survival pathways to unravel therapeutic options.Genetics and molecular biology · 2024Article
- Novel Approaches to Possible Targeted Therapies and Prophylaxis of Uterine Fibroids.Diseases (Basel, Switzerland) · 2023Review
- Article
- Wnt/β-catenin signaling pathway in uterine leiomyoma: role in tumor biology and targeting opportunities.Molecular and cellular biochemistry · 2021Review
- MicroRNA-182 is a potential biomarker for prognosis of gastric cancer: A protocol for meta-analysis and bioinformatics analysis.Medicine · 2021Article
- Article
- Activation of protein kinase B by WNT4 as a regulator of uterine leiomyoma stem cell function.Fertility and sterility · 2020Article
- 4D Genome Rewiring during Oncogene-Induced and Replicative Senescence.Molecular cell · 2020Article
- MiR-150-5p May Contribute to Pathogenesis of Human Leiomyoma via Regulation of the Akt/p27International journal of molecular sciences · 2019Article
- Mifepristone inhibits IGF-1 signaling pathway in the treatment of uterine leiomyomas.Drug design, development and therapy · 2019Article
- Application of ex-vivo spheroid model system for the analysis of senescence and senolytic phenotypes in uterine leiomyoma.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- Oxidative stress-induced miRNAs modulate AKT signaling and promote cellular senescence in uterine leiomyoma.Journal of molecular medicine (Berlin, Germany) · 2018Article
- Comparative analysis of AKT and the related biomarkers in uterine leiomyomas with MED12, HMGA2, and FH mutations.Genes, chromosomes & cancer · 2018Article
- The AKT/BCL-2 Axis Mediates Survival of Uterine Leiomyoma in a Novel 3D Spheroid Model.Endocrinology · 2018Article
- Asxl1 deficiency in embryonic fibroblasts leads to cellular senescence via impairment of the AKT-E2F pathway and Ezh2 inactivation.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Uterine leiomyomas (fibroids) are a major public health problem. Current medical treatments with GnRH analogs do not provide long-term benefit. Thus, permanent shrinkage or inhibition of fibroid growth via medical means remains a challenge. The AKT pathway is a major growth and survival pathway for fibroids. We propose that AKT inhibition results in a transient regulation of specific mechanisms that ultimately drive cells into cellular senescence or cell death. In this study, we investigated specific mechanisms of AKT inhibition that resulted in senescence. We observed that administration of MK-2206, an allosteric AKT inhibitor, increased levels of reactive oxygen species, up-regulated the microRNA miR-182 and several senescence-associated genes (including p16, p53, p21, and β-galactosidase), and drove leiomyoma cells into stress-induced premature senescence (SIPS). Moreover, induction of SIPS was mediated by HMGA2, which colocalized to senescence-associated heterochromatin foci. This study provides a conceivable molecular mechanism of SIPS by AKT inhibition in fibroids.
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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 OpenQuestion graph.