ArticleCell death & disease2026
Disrupting SRSF10-dependent BCAT2 exon skipping reprograms tumor-associated macrophages and enhances anti-PD-1 efficacy in gastric cancer.
Article in Cell death & disease, 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
Aberrant alternative splicing (AS) in cancer generates oncogenic proteomic diversity that drives tumor progression. Given the suboptimal efficacy of immune checkpoint inhibitors (ICIs) in gastric cancer (GC), the therapeutic potential of modulating RNA splicing to augment immunotherapy remains unclear. Here, we demonstrate that the splicing factor SRSF10 is progressively upregulated during gastric tumorigenesis and exhibits elevated expression in ICIs-resistant GC. Utilizing multiple mouse models, we confirmed that SRSF10 ablation with a selective inhibitor 1C8 robustly inhibits GC growth and enhances CD8
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