ArticlePloS one2011
Interleukin-22 suppresses the growth of A498 renal cell carcinoma cells via regulation of STAT1 pathway.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 27 citations in OpenAlex.
- Interleukin-22 promotes endometrial carcinoma cell proliferation and cycle progression via ERK1/2 and p38 activation.Molecular and cellular biochemistry · 2025Article
- Immune cell mediated cabozantinib resistance for patients with renal cell carcinoma.Integrative biology : quantitative biosciences from nano to macro · 2021Article
- Interleukin-22 promotes development of malignant lesions in a mouse model of spontaneous breast cancer.Molecular oncology · 2020Article
- Accumulation of T-helper 22 cells, interleukin-22 and myeloid-derived suppressor cells promotes gastric cancer progression in elderly patients.Oncology letters · 2018Article
- Melatonin alleviates inflammation-induced apoptosis in human umbilical vein endothelial cells via suppression of CaCell stress & chaperones · 2018Article
- Biological and pathological activities of interleukin-22.Journal of molecular medicine (Berlin, Germany) · 2016Review
- Article
- Interleukin-22: immunobiology and pathology.Annual review of immunology · 2015Review
- The bradykinin B(2) receptor induces multiple cellular responses leading to the proliferation of human renal carcinoma cell lines.Cancer management and research · 2012Article
- Association of interleukin 22 receptor subunit alpha 1 gene polymorphisms with chronic rhinosinusitis.Brazilian journal of otorhinolaryngologyArticle
- The crystal structure of zebrafish IL-22 reveals an evolutionary, conserved structure highly similar to that of human IL-22.Genes and immunityArticle
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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
backgroundRenal cell carcinoma (RCC) is one of the most common kidney cancers and is highly resistant to chemotherapy. Accumulating evidence suggests that interleukin-22 (IL-22) may mediate host defense against varietal pathogens as a proinflammatory and anti-inflammatory cytokine. The purpose of this study is to assess the inhibitory effects of IL-22 on human RCC cell line A498 and to investigate the possible mechanisms underlying the anti-tumor effects of this cytokine. METHODOLOGY: A498 cells, a RCC cell line, were used to assess the inhibitory growth effects of IL-22 using the MTT assay and flow cytometric analysis in vitro. BALB/C nude mice bearing A498 cell xenografts were used to examine the antitumor efficacy of IL-22 in vivo. Western blotting assay was performed to detect the regulation of the intracellular signaling pathway of IL-22. PRINCIPAL
findingsWe found that IL-22 suppressed the growth of A498 cells in a dose-dependent manner and inhibited the growth of A498 xenografts. We also observed that IL-22 produced a dose-dependent inhibitory effect on A498 cells that involved the induction of G2/M cell cycle arrest without cell apoptosis. Moreover, we showed that the phosphorylation of STAT1 was increased and the phosphorylation of ERK1/2 was attenuated in A498 cells exposed to IL-22. The growth inhibition of A498 cells was partially revised after IL-22 treatment as the expression of STAT1 was knocked down. And inflammatory cytokines, interferon-α and tumor necrosis factor-α (TNF-α) were barely involved in the suppression of A498 cell xenografts treated with IL-22.
conclusionsIL-22 dose-dependently suppresses RCC cell line A498 cells in vitro and induces growth inhibition of A498 cell-bearing mouse xenografts. These results suggest that the anti-RCC effects of IL-22 are at least partially mediated through regulation of STAT1 signaling pathways and G2/M cell cycle arrest, rather than by inducing apoptosis and inflammatory cytokines.
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