ArticleCancer cell international2026
IL-18 suppresses retinoblastoma growth while concomitantly inducing an inflammation-/stress-associated and immune-remodeling response.
Article in Cancer cell international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Retinoblastoma is the most common intraocular malignancy in childhood and remains associated with substantial treatment related morbidity. Interleukin 18 (IL-18) is an immunomodulatory cytokine with context dependent roles in cancer, yet its functional significance in retinoblastoma is unclear. Here, integrated transcriptomic analyses of GEO datasets revealed that retinoblastoma displays an immune exposed and stress associated transcriptional state and identified IL-18 as a consistently downregulated immune related cytokine across datasets. Functionally, exogenous IL-18 suppressed cell growth in Y79 and WERI-Rb1 retinoblastoma cells and promoted apoptotic commitment, as evidenced by reduced Bcl-2 and Bcl-xL together with increased Caspase-3, Bax, and Bad, and was further supported by Annexin V and PI flow cytometry. Notably, IL-18 induced growth inhibition co occurred with increased expression of selected inflammation and stress associated proteins. In vivo, xenografts derived from IL-18 pretreated cells exhibited reduced tumor burden, whereas IL-18 binding protein partially reversed these effects. Tumors from the IL-18 condition also showed elevated IL-6 and TNF-alpha and altered immune related markers, including increased CD4, CD8, and CD206 positive populations, indicating concurrent inflammatory and immune remodeling. Collectively, these data suggest that IL-18 exerts a net tumor restrictive effect in retinoblastoma models while concomitantly engaging inflammation and immune associated programs, highlighting IL-18 related modulation as a context dependent axis relevant to retinoblastoma progression.
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