ArticleJournal of experimental & clinical cancer research : CR2013
Everolimus-induced human keratinocytes toxicity is mediated by STAT3 inhibition.
Article in Journal of experimental & clinical cancer research : CR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Targeting CXCR2 in Nociceptive Sensory Neurons Offers Novel Therapeutic Potentials for Postoperative Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Oncostatin M upregulates CD73 via the MAPK pathway in keratinocytes to promote an adenosine-dependent anti-inflammatory response in psoriasis.Frontiers in immunology · 2026Article
- Signal-transducing adaptor protein 1 (STAP1) in microglia promotes the malignant progression of glioma.Journal of neuro-oncology · 2023Article
- Analysis of the synergistic antifungal activity of everolimus and antifungal drugs against dematiaceous fungi.Frontiers in cellular and infection microbiology · 2023Article
- Article
- Myostatin regulates pituitary development and hepatic IGF1.American journal of physiology. Endocrinology and metabolism · 2019Article
- Impact on Autophagy and Ultraviolet B Induced Responses of Treatment with the MTOR Inhibitors Rapamycin, Everolimus, Torin 1, and pp242 in Human Keratinocytes.Oxidative medicine and cellular longevity · 2017Article
- Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMammalian target of rapamycin (mTOR) inhibitors are associated with dermatological adverse events. The chief aim of this study was to examine the relation between the signal transducer and activator of transcription 3 (STAT3) protein and the dermatological adverse events associated with the mTOR inhibitor everolimus.
methodsWe evaluated the effects of STAT3 activity and related signal transduction activities on everolimus-induced cell growth inhibition in the human keratinocyte HaCaT cell line via a WST-8 assay, and on signal transduction mechanisms involved in everolimus treatments via a western blot analysis. Apoptosis was evaluated using an imaging cytometric assay.
resultsThe cell growth inhibitory effects of everolimus were enhanced by stattic or STA-21, which are selective inhibitors of STAT3, treatment in HaCaT cells, although such effects were not observed in Caki-1 and HepG2 cells. Phosphorylation at tyrosine 705 of STAT3 was decreased by treatment with everolimus in a dose-dependent manner in HaCaT cells; in contrast, phosphorylation at serine 727 was not decreased by everolimus, but slightly increased. Furthermore, we found that pretreatment of p38 MAPK inhibitor and transfection with constitutively active form of STAT3 in HaCaT cells resisted the cytostatic activity of everolimus.
conclusionsThese findings suggest that STAT3 activity may be a biomarker of everolimus-induced dermatological toxicity.
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