ArticleScientific reports2025
Apatinib-Induced STAT1/NK axis activation augments PD-1 inhibitor efficacy in advanced Hepatocellular Carcinoma.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
10 authors.
Funding
Abstract
The combination of immune checkpoint inhibitors (ICIs) with anti-angiogenic agents has demonstrated efficacy in the clinical treatment of advanced hepatocellular carcinoma (HCC). This study seeks to elucidate the underlying mechanisms that contribute to the enhanced therapeutic effects of apatinib when administered in conjunction with ICIs for the treatment of advanced HCC. The effects of apatinib on the viability, clonal formation, and apoptosis of HCC cells were evaluated through in vitro experiments. Meanwhile, in vivo experiments were conducted to substantiate these findings and further investigate the synergistic effects of apatinib with PD-1 inhibitors on the immune microenvironment, particularly by activating the signal transducer and activator of transcription 1 (STAT1)/natural killer (NK) cell axis. In vitro experiments demonstrated that apatinib significantly suppressed HCC cell viability, colony formation capacity, and induced apoptosis. In tumor-bearing mouse models, the combination of apatinib with PD-1 inhibitors showed superior tumor growth inhibition compared to monotherapy (combination group exhibited the smallest tumor volume and 100% survival rate vs. 0% in PBS group, p < 0.001). Western blot and immunohistochemical analyses revealed STAT1/NK axis activation through combination therapy (upregulated STAT1 expression with increased CD8
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