ArticleOncogene2006
Chronic UVA irradiation of human HaCaT keratinocytes induces malignant transformation associated with acquired apoptotic resistance.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 91 citations in OpenAlex.
- Trial
- Generation of cellular reactive oxygen and nitrogen species by exposure to ultraviolet radiation.Biophysical reviews · 2025Review
- MicroRNA31 and MMP-1 contribute to the differentiated pathway of invasion -with enhanced epithelial-to-mesenchymal transition- in squamous cell carcinoma of the skin.Archives of dermatological research · 2022Article
- The Antioxidant Activity of a Commercial and a Fractionated Phycocyanin on Human Skin Cells In Vitro.Molecules (Basel, Switzerland) · 2022Article
- Photoaging and Sequential Function Reversal with Cellular-Resolution Optical Coherence Tomography in a Nude Mice Model.International journal of molecular sciences · 2022Article
- Genomic Adaption and Mutational Patterns in a HaCaT Subline Resistant to Alkylating Agents and Ionizing Radiation.International journal of molecular sciences · 2021Article
- Xeroderma Pigmentosum C: A Valuable Tool to Decipher the Signaling Pathways in Skin Cancers.Oxidative medicine and cellular longevity · 2021Review
- Recent Updates on the Involvement of PI3K/AKT/mTOR Molecular Cascade in the Pathogenesis of Hyperproliferative Skin Disorders.Frontiers in medicine · 2021Review
- Hydrochlorothiazide Use and Risk of Nonmelanoma Skin Cancers: A Biological Plausibility Study.Oxidative medicine and cellular longevity · 2021Article
- Phosphorylation of xeroderma pigmentosum group C regulates ultraviolet-induced DNA damage repair.Nucleic acids research · 2018Article
- The effects of phototherapy and melanocytes on keratinocytes.Experimental and therapeutic medicine · 2018Article
- Phosphoinositide 3-Kinase-Dependent Signalling Pathways in Cutaneous Squamous Cell Carcinomas.Cancers · 2017Review
- Autophagy in UV Damage Response.Photochemistry and photobiology · 2017Review
- Development and Characterization of a Novel in vitro Progression Model for UVB-Induced Skin Carcinogenesis.Scientific reports · 2015Article
- SIRT6 promotes COX-2 expression and acts as an oncogene in skin cancer.Cancer research · 2014Article
- Suppression of PTEN transcription by UVA.Journal of biochemical and molecular toxicology · 2013Article
- UVA irradiation of dysplastic keratinocytes: oxidative damage versus antioxidant defense.International journal of molecular sciences · 2012Article
- UVA-induced DNA double-strand breaks result from the repair of clustered oxidative DNA damages.Nucleic acids research · 2012Article
- Resveratrol-sensitized UVA induced apoptosis in human keratinocytes through mitochondrial oxidative stress and pore opening.Journal of photochemistry and photobiology. B, Biology · 2012Article
- Overabundance of putative cancer stem cells in human skin keratinocyte cells malignantly transformed by arsenic.Toxicological sciences : an official journal of the Society of Toxicology · 2012Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Ultraviolet A (UVA, 315-400 nm), constituting about 95% of ultraviolet irradiation in natural sunlight, represents a major environmental challenge to the skin and is clearly associated with human skin cancer. It has proven difficult to show direct actions of UVA as a carcinogen in human cells. Here, we demonstrate that chronic UVA exposures at environmentally relevant doses in vitro can induce malignant transformation of human keratinocytes associated with acquired apoptotic resistance. As evidence of carcinogenic transformation, UVA-long-treated (24 J/cm(2) once/week for 18 weeks) HaCaT (ULTH) cells showed increased secretion of matrix metalloproteinase (MMP-9), overexpression of keratin 13, altered morphology and anchorage-independent growth. Malignant transformation was established by the production of aggressive squamous cell carcinomas after inoculation of ULTH cells into nude mice (NC(r)-nu). ULTH cells were resistant to apoptosis induced not only by UVA but also by UVB and arsenite, two other human skin carcinogens. ULTH cells also became resistant to apoptosis induced by etoposide, staurosporine and doxorubicin hydrochloride. Elevated phosphorylation of protein kinase B (PKB, also called AKT) and reduced expression of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) were detected in ULTH cells. The resistance of ULTH cells to UVA-induced apoptosis was reversed by either inhibition of phosphatidylinositol 3-kinase (PI-3K) or adenovirus expression of PTEN or dominant negative AKT. These data indicate that UVA has carcinogenic potential in human keratinocytes and that the increased AKT signaling and decreased PTEN expression may contribute to this malignant transformation. Further comparisons between the transformed ULTH and control cells should lead to a better understanding of the mechanism of UVA carcinogenesis and may help identify biomarkers for UVA-induced skin malignancies.
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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.