ArticleMycopathologia2009
Activation of ERK-FAK signaling pathway and enhancement of cell migration involved in the early interaction between oral keratinocytes and Candida albicans.
Article in Mycopathologia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Oral Microbiota-Driven Cell Migration in Carcinogenesis and Metastasis.Frontiers in cellular and infection microbiology · 2022Review
- Antifungal Effect of Long Noncoding RNA 9708-1 in the Vulvovaginal Candidiasis Murine Model.Mycopathologia · 2021Article
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- Article
- The Role of 17β-Estrogen in Candida albicans Adhesion on Human Vaginal Epithelial Cells via FAK Phosphorylation.Mycopathologia · 2020Article
- Novel naphthochalcone derivative accelerate dermal wound healing through induction of epithelial-mesenchymal transition of keratinocyte.Journal of biomedical science · 2015Article
- Candida albicans and Candida parapsilosis rapidly up-regulate galectin-3 secretion by human gingival epithelial cells.Mycopathologia · 2014Article
- Adrenergic signaling in human oral keratinocytes and wound repair.Journal of dental research · 2011Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposesTo investigate the early molecular events in oral keratinocytes induced by Candida albicans challenge.
methodsThe oral keratinocyte cell line, Tca8113, was used to study the molecular events induced by C. albicans challenge in oral keratinocytes. The phosphorylation statuses of extracellular signal-regulated protein kinase (ERK) and focal adhesion kinase (FAK) upon C. albicans challenge were assessed using specific antibodies and western blotting. Specific inhibitors for ERK and FAK were used to validate the involvement of ERK-FAK signaling cascade. A Transwell insert system-based migration study was performed to evaluate the involvement of the C. albicans-dependent ERK-FAK activation with cell migration.
resultsFollowing the stimulation with C. albicans, a transient activation of ERK was observed, which reached a peak at 10 min post stimulation. Similarly, a transient activation of FAK, the downstream substrate of ERK, was also observed upon C. albicans challenges, which reach the maximum at 20 min. Specific inhibitors for ERK and FAK abolished the C. albicans-induced ERK and FAK activations. The elevated migratory ability of oral keratinocyte was observed upon stimulation with C. albicans, and was synchronous with the ERK-FAK activation.
conclusionERK-FAK signaling cascades are involved in the early interaction between the oral keratinocytes and C. albicans, which appears to be linked with the enhanced cell migration.
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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 Socratic graph.