ArticleTranslational lung cancer research2026
TLR7 induces autophagy in non-small cell lung cancer tumor cells and influences anti-tumors responses in patients.
Article in Translational lung cancer research, 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
Background: Autophagy is a fundamental catabolic process with context-dependent roles in cancer. In non-small cell lung cancer (NSCLC), its clinical significance and therapeutic implications remain unclear. Toll-like receptor 7 (TLR7) has been implicated in the modulation of tumor-immune interactions, but its connection to autophagy and treatment response has not been defined. Here, we aimed to investigate whether TLR7 signaling regulates autophagy in NSCLC and to determine its impact on tumor progression and therapeutic responses. Methods: We combined transcriptomic analyses of multiple NSCLC patient cohorts with in vitro and ex vivo functional assays to investigate the relationship between TLR7 activation and autophagy. Gene expression profiling was used to assess the presence of TLR7 ligands and autophagy signatures in the tumor microenvironment (TME). Associations between tumor autophagy levels, clinical outcomes, and therapeutic responses were evaluated retrospectively in independent cohorts. Results: Our analyses revealed that endogenous TLR7 ligands are present in the NSCLC TME, where they activate autophagy in malignant cells. High tumor TLR7-dependent autophagy was associated with poor prognosis and reduced sensitivity to platinum-based chemotherapy. Conversely, elevated autophagy correlated with improved responses to nivolumab, an anti-programmed death-1 (PD-1) immunotherapy. Mechanistic studies demonstrated that TLR7-induced autophagy promotes resistance to cisplatin (Cis.) and oxaliplatin (Oxali.) while upregulating PD-L1 expression, establishing a direct link between autophagy and therapeutic outcomes. Conclusions: These findings identify TLR7-driven autophagy as a novel pathogenic pathway in NSCLC and a clinically relevant determinant of treatment response. This mechanism provides new insight into how tumor-intrinsic innate signaling shapes sensitivity to chemotherapy and immunotherapy, offering potential targets for therapeutic modulation.
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