ArticleChinese medicine2026
Shuangshen granules enhance anti-PD1 therapy effectiveness in lung adenocarcinoma by modulating myeloid-derived suppressor cell-induced T cell exhaustion.
Article in Chinese 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
backgroundWorldwide, lung cancer is the most common cause of cancer-related deaths. Molecular targeted therapies and immunotherapies for non-small-cell lung cancer (NSCLC) have improved outcomes markedly over the past two decades. However, the vast majority of advanced NSCLCs become resistant to current treatments and eventually progress. A traditional Chinese medicine (TCM) formula of Shuangshen granules (SSG) has demonstrated potential in alleviating cancer side effects and improving survival rate. Despite clinical evidence supporting its benefit, there is still insufficient understanding of the active compounds in SSG and their underlying mechanisms, which limits its broader clinical application.
methodsLewis lung carcinoma (LLC) tumor-bearing mouse model was established to assess the efficacy of combined SSG and anti-PD-1 therapy in vivo, and myeloid-derived suppressor cells (MDSC) and CD8
resultsIn vivo experiments using LLC xenograft mice demonstrated that SSG suppressed tumor growth in a dose-dependent manner, with high-dose SSG showing optimal efficacy in inhibiting tumor angiogenesis and cell proliferation. SSG enhances anti-tumor immunity by reducing T cell exhaustion and MDSC-mediated immunosuppression, with SSG + anti-PD-1 combination therapy synergistically optimizing the tumor immune microenvironment. Network pharmacology analysis revealed 5 hub targets (IL2, STAT3, HSP90AA1, LGALS3, and FGF2) associated with immune, LUAD, and active ingredients of SSG, with significant enrichment in the PI3K-Akt pathway. Compared with the control group, the protein expression levels of p-PI3K and p-Akt in the SSG group were significantly down-regulated, indicating that the PI3K-Akt pathway may be inhibited.
conclusionsSSG could dose-dependently inhibit LLC tumor growth in mice and exert antitumor effects by alleviating T-cell exhaustion and MDSC-mediated immunosuppression. Notably, IL2, STAT3, HSP90AA1, LGALS3 and FGF2, as potential targets of SSG, were significantly enriched in the PI3K-Akt pathway, which provide a novel perspective for the treatment of LUAD.
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