ArticleNature communications2022
Targeting anti-apoptotic pathways eliminates senescent melanocytes and leads to nevi regression.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- Skin Aging: From Molecular Mechanisms to Therapeutic and Technological Innovations.Journal of cellular and molecular medicine · 2026Review
- Inhibition of Aurora B induces senescence and potentiates immunotherapy in hepatocellular carcinoma.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Mitochondrial bioenergetics-SASP crosstalk determines senolytic efficacy in therapy-induced senescence.Cell death discovery · 2026Article
- Silencing myeloid cell leukemia-1 improves apoptotic and ferroptotic responses in melanoma.European journal of medical research · 2026Article
- Biomaterials targeting senescent cells for bone regeneration: State-of-the-art and future perspectives.Bioactive materials · 2025Review
- Demystifying programmed cell death in lung adenocarcinoma: combined prognostic model construction.Translational cancer research · 2025Article
- Apoptotic priming in senescence predicts specific senolysis by quantitative analysis of mitochondrial dependencies.Cell death and differentiation · 2025Article
- Senolysis by ABT-263 is associated with inherent apoptotic dependence of cancer cells derived from the non-senescent state.Cell death and differentiation · 2025Article
- HRK downregulation and augmented BCL-xL binding to BAK confer apoptotic protection to therapy-induced senescent melanoma cells.Cell death and differentiation · 2025Article
- Mitochondrial priming and response to BH3 mimetics in "one-two punch" senogenic-senolytic strategies.Cell death discovery · 2025Article
- A galactose-tethered tetraphenylethene prodrug mediated apoptosis of senescent cells for osteoporosis treatment.Science advances · 2025Article
- Cellular Senescence in Health, Disease, and Lens Aging.Pharmaceuticals (Basel, Switzerland) · 2025Review
- The three barriers senescent tumor cells must overcome to relapse.Cancer heterogeneity and plasticity · 2025Article
- Mitochondrial priming in therapy-induced senescence: implications for CAR-T/NK immunosenolytic therapy.Frontiers in immunology · 2025Review
- Topical ABT-263 treatment reduces aged skin senescence and improves subsequent wound healing.Aging · 2024Article
- MYO6 contributes to tumor progression and enzalutamide resistance in castration-resistant prostate cancer by activating the focal adhesion signaling pathway.Cell communication and signaling : CCS · 2024Article
- Review
- Mild Uncoupling of Mitochondria Synergistically Enhances Senolytic Specificity and Sensitivity of BH3 Mimetics.Aging biology · 2024Article
- Modulation of tumor plasticity by senescent cells: Deciphering basic mechanisms and survival pathways to unravel therapeutic options.Genetics and molecular biology · 2024Article
- Death-seq identifies regulators of cell death and senolytic therapies.Cell metabolism · 2023Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Human melanocytic nevi (moles) result from a brief period of clonal expansion of melanocytes. As a cellular defensive mechanism against oncogene-induced hyperplasia, nevus-resident melanocytes enter a senescent state of stable cell cycle arrest. Senescent melanocytes can persist for months in mice and years in humans with a risk to escape the senescent state and progress to melanoma. The mechanisms providing prolonged survival of senescent melanocytes remain poorly understood. Here, we show that senescent melanocytes in culture and in nevi express high level of the anti-apoptotic BCL-2 family member BCL-W but remain insensitive to the pan-BCL-2 inhibitor ABT-263. We demonstrate that resistance to ABT-263 is driven by mTOR-mediated enhanced translation of another anti-apoptotic member, MCL-1. Strikingly, the combination of ABT-263 and MCL-1 inhibitors results in synthetic lethality to senescent melanocytes, and its topical application sufficient to eliminate nevi in male mice. These data highlight the important role of redundant anti-apoptotic mechanisms for the survival advantage of senescent melanocytes, and the proof-of-concept for a non-invasive combination therapy for nevi removal.
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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.