ArticleInternational journal of oncology2012
STAT3 signal transduction through interleukin-22 in oral squamous cell carcinoma.
Article in International journal of oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- Interleukin-22 promotes endometrial carcinoma cell proliferation and cycle progression via ERK1/2 and p38 activation.Molecular and cellular biochemistry · 2025Article
- The role of IL-22 in cancer.Medical oncology (Northwood, London, England) · 2024Review
- IL-6/JAK2-dependent G6PD phosphorylation promotes nucleotide synthesis and supports tumor growth.Molecular metabolism · 2023Article
- Research progress on Th22 cells and related cytokines in tumors: current status and future perspectives.American journal of cancer research · 2023Review
- Review
- The multifaceted role of STAT3 pathway and its implication as a potential therapeutic target in oral cancer.Archives of pharmacal research · 2022Review
- The origin of bladder cancer from mucosal field effects.iScience · 2022Article
- Molecular Pathogenesis of Psoriasis and Biomarkers Reflecting Disease Activity.Journal of clinical medicine · 2021Review
- Identification of oral squamous cell carcinoma markers MUC2 and SPRR1B downstream of TANGO.Journal of cancer research and clinical oncology · 2021Article
- Role of Th22 Cells in the Pathogenesis of Autoimmune Diseases.Frontiers in immunology · 2021Review
- Tissue Damage in Radiation-Induced Oral Mucositis Is Mitigated by IL-17 Receptor Signaling.Frontiers in immunology · 2021Article
- Interleukin-22 enhances chemoresistance of lung adenocarcinoma cells to paclitaxel.Human cell · 2020Article
- p38 Expression and Modulation of STAT3 Signaling in Oral Cancer.Pathology oncology research : POR · 2020Article
- STAT3 activation by E6 is essential for the differentiation-dependent HPV18 life cycle.PLoS pathogens · 2018Article
- IL-22 suppresses the infection of porcine enteric coronaviruses and rotavirus by activating STAT3 signal pathway.Antiviral research · 2017Article
- Interleukin 22 attenuated angiotensin II induced acute lung injury through inhibiting the apoptosis of pulmonary microvascular endothelial cells.Scientific reports · 2017Article
- SOCS3 inhibits the pathological effects of IL-22 in non-melanoma skin tumor-derived keratinocytes.Oncotarget · 2017Article
- Role of tumour-associated macrophages in oral squamous cells carcinoma progression: an update on current knowledge.Diagnostic pathology · 2017Review
- JNK1/2 expression and modulation of STAT3 signaling in oral cancer.Oncology letters · 2016Article
- Biological and pathological activities of interleukin-22.Journal of molecular medicine (Berlin, Germany) · 2016Review
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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
Interleukin (IL)-22 is a member of the IL-10 family. Its main targets are epithelial cells, not immune cells. We examined IL-22 signal transduction in oral squamous cell carcinoma (OSCC) cells. Immunohistochemical staining revealed that IL-22R was expressed more highly in OSCC compared to normal regions. An IL-22R signal was also observed in metastatic OSCC cells in the lymph node. RT-PCR showed that the human OSCC cell lines MISK81-5, HSC-3, HSC-4, SAS and SQUU-B expressed IL-22 receptor chains. Immunoblotting showed that IL-22 induced a transient tyrosine phosphorylation of STAT3 (pY705-STAT3) in MISK81-5 cells. The change in the serine phosphorylation of STAT3 was subtle during the examination periods. Simultaneously, pY705-STAT3 activation in HSC-3 cells was undetectable after IL-22 stimulation. Immunocytochemistry demonstrated that IL-22 induced the translocation of phosphorylated STAT3 into the nucleus of MISK81-5 cells. IL-22 temporarily upregulated the expression of anti-apoptotic and mitogenic genes such as Bcl-x, survivin and c-Myc, as well as SOCS3. IL-22 transiently activated ERK1/2 and induced a delayed phosphorylation of p38 MAP kinase, but negligibly involved the activation of NF-κB in MISK81-5 cells. MISK81-5 and SQUU-B cells treated with IL-22 showed mild cellular proliferation. MISK81-5, HSC-4 and SAS cells treated with IL-22 downregulated the keratinocyte differentiation-related genes compared with unstimulated cells. Conversely, STAT3 suppression by STAT3 siRNA strongly disrupted the downregulation of these genes by IL-22, but it did not significantly affect the activation of ERK1/2 by IL-22. The OSCC cells used in this study upregulated the expression of SERPINB3/4 (SCCA1/2), well-known SCC markers, following treatment with IL-22. These results indicate that IL-22 differentially activates the STAT3 signaling system depending on the type of OSCC. IL-22 may therefore play a role in tumor growth, cell differentiation and progression through STAT3-dependent and -independent pathways.
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