ArticleScience advances2016
Dysfunctional MnSOD leads to redox dysregulation and activation of prosurvival AKT signaling in uterine leiomyomas.
Article in Science advances, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 48 citations in OpenAlex.
- The estrogen-progestogen-oxidative stress network in uterine fibroids: mechanistic insights and therapeutic opportunities.Redox report : communications in free radical research · 2026Review
- Human Myometrial Cell Fate under Chronic Oxidative Stress for Leiomyomagenesis.Research square · 2026Article
- Oxidative stress-triggered UMPylation of SodA by YdiU modulates oxidative stress resistance in Salmonella.Veterinary research · 2026Article
- Correlation Between Superoxide Dismutase and Very-Low-Density Lipoprotein Cholesterol in the Blood of Patients with Uterine Fibroids.International journal of women's health · 2026Article
- Metals and metal mixtures associated with the odds of uterine fibroid prevalence among African Caribbean women in the Tobago Health Study.Frontiers in reproductive health · 2026Article
- UTERINE FIBROIDS.Physiological reviews · 2025Review
- Superoxide Dismutases in Immune Regulation and Infectious Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Body Mass Index and Uterine Fibroid Development: A Prospective Study.The Journal of clinical endocrinology and metabolism · 2024Article
- The Impact of High Adiposity on Endometrial Progesterone Response and Metallothionein Regulation.The Journal of clinical endocrinology and metabolism · 2024Article
- SomaticCells · 2024Article
- Hypoxia in uterine fibroids: role in pathobiology and therapeutic opportunities.Oxygen (Basel, Switzerland) · 2024Article
- Racial disparity in uterine leiomyoma: new insights of genetic and environmental burden in myometrial cells.Molecular human reproduction · 2024Review
- NIPSNAP1 directs dual mechanisms to restrain senescence in cancer cells.Journal of translational medicine · 2023Article
- Racial differences in transcriptomics and reactive oxygen species burden in myometrium and leiomyoma.Human reproduction (Oxford, England) · 2023Article
- Oxidative Stress and Antioxidants in Uterine Fibroids: Pathophysiology and Clinical Implications.Antioxidants (Basel, Switzerland) · 2023Review
- High SPATA18 Expression and its Diagnostic and Prognostic Value in Clear Cell Renal Cell Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2023Article
- Maternal Metals Exposure and Infant Weight Trajectory: The Japan Environment and Children's Study (JECS).Environmental health perspectives · 2022Article
- Myometrial oxidative stress drives MED12 mutations in leiomyoma.Cell & bioscience · 2022Article
- Manganese Superoxide Dismutase Acetylation and Regulation of Protein Structure in Breast Cancer Biology and Therapy.Antioxidants (Basel, Switzerland) · 2022Review
- Targeting prooxidant MnSOD effect inhibits triple-negative breast cancer (TNBC) progression and M2 macrophage functions under the oncogenic stress.Cell death & disease · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
AKT signaling promotes cell growth and survival and is often dysregulated via multiple mechanisms in different types of cancer, including uterine leiomyomas (ULMs). ULMs are highly prevalent fibrotic tumors that arise from the smooth muscular layer of the uterus, the myometrium (MM). ULMs pose a major public health issue because they can cause severe morbidity and poor pregnancy outcomes. We investigate the mechanisms driving ULM growth and survival via aberrant activation of AKT. We demonstrate that an acetylation-mediated impairment of the manganese superoxide dismutase (MnSOD) activity is prevalent in ULM cells compared to the normal-matched MM from the same patients. This impairment increases the levels of superoxide and oxidative stress, which activate AKT via oxidative inactivation of the phosphatase and tensin homolog deleted on chromosome 10 (PTEN). Redox activation of AKT promotes ULM cell survival under conditions of moderate but persistent oxidative stress that are compatible with ULM's prooxidative microenvironment. Moreover, because of impaired MnSOD activity, ULM cells are sensitive to high levels of reactive oxygen species (ROS) and superoxide-generating compounds, resulting in decreased ULM cell viability. On the contrary, MM cells with functional MnSOD are more resistant to high levels of oxidants. This study demonstrates a causative role of acetylation-mediated MnSOD dysfunction in activating prosurvival AKT signaling in ULMs. The specific AKT and redox states of ULM cells provide a potential novel therapeutic rationale to selectively target ULM cells because of their defective ROS-scavenging system..
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