ArticleCell death & disease2014
Level of macroautophagy drives senescent keratinocytes into cell death or neoplastic evasion.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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
22 citing papers in PubMed, 36 citations in OpenAlex.
- Biallelic GLTP mutations cause nonsyndromic epidermal differentiation disorder via disrupted epidermal glucosylceramide transport.The Journal of clinical investigation · 2026Article
- Interplay between MAPK signaling pathway and autophagy in skin aging: mechanistic insights and therapeutic implications.Frontiers in cell and developmental biology · 2025Review
- Prostaglandin EAging · 2024Article
- The multifaceted role of autophagy in skin autoimmune disorders: a guardian or culprit?Frontiers in immunology · 2024Review
- Aldehyde Dehydrogenase Genes as Prospective Actionable Targets in Acute Myeloid Leukemia.Genes · 2023Article
- Skin Cancer Microenvironment: What We Can Learn from Skin Aging?International journal of molecular sciences · 2023Review
- Flow Cytometry-based Method for Efficient Sorting of Senescent Cells.Bio-protocol · 2023Article
- The Epidermal Keratinocyte as a Therapeutic Target for Management of Diabetic Wounds.International journal of molecular sciences · 2023Review
- Review
- Proteasome-mediated degradation of keratins 7, 8, 17 and 18 by mutant KLHL24 in a foetal keratinocyte model: Novel insight in congenital skin defects and fragility of epidermolysis bullosa simplex with cardiomyopathy.Human molecular genetics · 2022Article
- Skin Pigmentation Abnormalities and Their Possible Relationship with Skin Aging.International journal of molecular sciences · 2021Review
- Role of constitutive nitric oxide synthases in the dynamic regulation of the autophagy response of keratinocytes upon UVB exposure.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2020Article
- Chemotherapy-induced senescence, an adaptive mechanism driving resistance and tumor heterogeneity.Cell cycle (Georgetown, Tex.) · 2019Review
- Autophagic Control of Skin Aging.Frontiers in cell and developmental biology · 2019Review
- High Glucose Suppresses Keratinocyte Migration Through the Inhibition of p38 MAPK/Autophagy Pathway.Frontiers in physiology · 2019Article
- Autophagy and the cell biology of age-related disease.Nature cell biology · 2018Review
- Regulation of senescence escape by the cdk4-EZH2-AP2M1 pathway in response to chemotherapy.Cell death & disease · 2018Article
- Epithelial cell senescence: an adaptive response to pre-carcinogenic stresses?Cellular and molecular life sciences : CMLS · 2017Review
- Unlocking the chromatin of adenoid cystic carcinomas using HDAC inhibitors sensitize cancer stem cells to cisplatin and induces tumor senescence.Stem cell research · 2017Article
- Defective DNA single-strand break repair is responsible for senescence and neoplastic escape of epithelial cells.Nature communications · 2016Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Senescence is a non-proliferative state reached by normal cells in response to various stresses, including telomere uncapping, oxidative stress or oncogene activation. In previous reports, we have highlighted that senescent human epidermal keratinocytes have two opposite outcomes: either they die by autophagic programmed cell death or they evade in the form of neoplastic postsenescence emergent (PSNE) cells. Herein, we show that partially reducing macroautophagy in senescent keratinocytes using 3-methyl adenine or anti-Atg5 siRNAs increases the PSNE frequency, suggesting that senescent keratinocytes have to escape autophagic cell death to generate PSNE cells. However, totally inhibiting macroautophagy impairs PSNE and leads to a huge accumulation of oxidative damages, indicating that senescent keratinocytes need to achieve quality-control macroautophagy for PSNE to occur. In accordance, we demonstrate that the progenitors of PSNE cells display a level of macroautophagy slightly lower than that of the average senescent population, which is directly dictated by their level of reactive oxygen species, their level of upregulation of MnSOD, their level of activation of NF-κB transcription factors and their level of dysfunctional mitochondria. Macroautophagy thus has antagonistic roles during senescence, inducing cell death or promoting neoplastic transformation, depending on its level of activation. Taken together, these data suggest that levels of oxidative damages and ensuing macroautophagic activity could be two main determinants of the very initial phases of neoplastic transformation by senescence evasion.
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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.