ArticleNPJ precision oncology2026
SNORD50A/B disassemble ASC-1 complex to silence NF-κB and boost PD-1 blockade in non-small-cell lung cancer.
Article in NPJ precision oncology, 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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10 authors.
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Abstract
Small nucleolar RNA SNORD50A and SNORD50B (SNORD50A/B) have increasingly been linked to tumorigenesis due to their high frequency of deletion across multiple cancer types. However, their biological roles in non-small-cell lung cancer (NSCLC) remain to be systematically investigated. In this study, we observed that SNORD50A/B were frequently deleted in lung adenocarcinomas, and this molecular event was strongly linked to poor patient survival. Subsequent in vitro and in vivo studies demonstrated the tumor-suppressive role of SNORD50A/B in NSCLC. Mechanistically, SNORD50A/B directly bound to activating signal cointegrator 1 complex subunit 1 (ASCC1), preventing its interaction with activating signal cointegrator 1 (ASC-1) and disrupting the integrity of ASC-1 complex, which attenuates NF-κB transcriptional activity and down-regulates PD-L1 expression. Synthetic Snord50a/b-loaded cationic liposomes showed potent anti-tumor effects and sensitized NSCLC cells to anti-PD-1 immunotherapy. Taken together, SNORD50A/B exert tumor-suppressive effects by disrupting the ASC-1 complex to silence NF-κB, highlighting its therapeutic potential via cationic liposomes for treating SNORD50A/B-deficient tumors.
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