ArticleCancer biology & medicine2026
Antitumor effects of STING agonists on nervous system tumors via tumor-intrinsic STING-STAT1-mediated HMGN2 expression.
Article in Cancer biology & medicine, 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
objectiveClinical use of stimulator of interferon genes (STING) agonists has challenges due to poor responsiveness and variable efficacy. Therefore, identifying tumor types that are sensitive to these agents and clarifying the underlying mechanisms are essential.
methods
resultsNeuroblastomas and glioblastomas, two nervous system tumors, were shown to be sensitive to STING agonists. SR-717 exhibited greater antitumor efficacy compared to E7766. Mechanistic studies indicated that STING agonists promote apoptosis through activation of the intrinsic STING-signal transducer and activator of transcription 1 (STAT1)-HMGN2 axis within tumor cells. Ectopic expression of HMGN2 in melanoma cells, which naturally lack HMGN2, led to significant apoptosis. Furthermore, analysis of The Cancer Genome Atlas and Gene Expression Omnibus databases revealed positive correlation between elevated HMGN2 expression and patient survival, supporting the utility of HMGN2 as a prognostic biomarker.
conclusionsThis study clarified the mechanism underlying the potent antitumor activity of SR-717 in nervous system tumors through activation of the STING-STAT1-HMGN2 signaling pathway and demonstrated that SR-717 has superior efficacy compared to E7766. In addition, HMGN2 was shown to exhibit translational potential as a prognostic biomarker for patient survival.
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