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Published on: April 3, 2026

SNORD50A/B disassemble ASC-1 complex to silence NF-κB and boost PD-1 blockade in non-small-cell lung cancer

Jingjing Ma1,2, Qingyuan He1,2, Jun Pu1,2

  • 1Department of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.

NPJ Precision Oncology
|May 25, 2026
PubMed

Insights

Small nucleolar RNA SNORD50A/B are tumor suppressors in non-small-cell lung cancer (NSCLC). Deletion of SNORD50A/B correlates with poor survival, but liposomal delivery shows therapeutic promise.

Area of Science:

  • Oncology
  • Molecular Biology
  • RNA Biology

Background:

  • Small nucleolar RNAs SNORD50A and SNORD50B (SNORD50A/B) are frequently deleted in various cancers.
  • Their specific roles in non-small-cell lung cancer (NSCLC) require detailed investigation.

Purpose of the Study:

  • To investigate the biological functions and therapeutic potential of SNORD50A/B in NSCLC.
  • To elucidate the molecular mechanisms underlying SNORD50A/B's role in NSCLC tumorigenesis.

Main Methods:

  • Analysis of SNORD50A/B deletion frequency and correlation with survival in lung adenocarcinoma patients.
  • In vitro and in vivo experiments to assess the tumor-suppressive role of SNORD50A/B.
  • Mechanistic studies involving interactions with ASCC1, ASC-1 complex, NF-κB, and PD-L1 expression.
  • Evaluation of synthetic SNORD50A/B-loaded cationic liposomes for anti-tumor effects and immunotherapy sensitization.

Main Results:

  • SNORD50A/B deletions are frequent in lung adenocarcinomas and linked to poor patient survival.
  • SNORD50A/B exhibit tumor-suppressive functions in NSCLC.
  • SNORD50A/B inhibit the ASC-1 complex, reduce NF-κB activity, and down-regulate PD-L1 expression.
  • SNORD50A/B-loaded liposomes demonstrate potent anti-tumor efficacy and enhance anti-PD-1 therapy response.

Conclusions:

  • SNORD50A/B act as tumor suppressors in NSCLC by disrupting the ASC-1 complex and inhibiting NF-κB signaling.
  • Targeted delivery of SNORD50A/B using cationic liposomes presents a promising therapeutic strategy for SNORD50A/B-deficient NSCLC.

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