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MOSS: Self-Evolution through Source-Level Rewriting in Autonomous Agent Systems
Correction: Integrative multi-omics and machine learning reveals the spatial niche distribution and role of CYP27A1+TAMs in immunotherapy response in non-small cell lung cancer
Front Immunol. 2026 Mar 16;17:1822612. doi: 10.3389/fimmu.2026.1822612. eCollection 2026.
ABSTRACT
[This corrects the article DOI: 10.3389/fimmu.2026.1782545.].
PMID:41918731 | PMC:PMC13033988 | DOI:10.3389/fimmu.2026.1822612
Correction: Integrative multi-omics and machine learning reveals the spatial niche distribution and role of CYP27A1+TAMs in immunotherapy response in non-small cell lung cancer
Front Immunol. 2026 Mar 16;17:1822612. doi: 10.3389/fimmu.2026.1822612. eCollection 2026.
ABSTRACT
[This corrects the article DOI: 10.3389/fimmu.2026.1782545.].
PMID:41918731 | PMC:PMC13033988 | DOI:10.3389/fimmu.2026.1822612
RFC4 drives temozolomide resistance in glioblastoma by activating STK38-BECN1-dependent autophagy
Nat Commun. 2026 Mar 23. doi: 10.1038/s41467-026-70798-1. Online ahead of print.
ABSTRACT
Glioblastoma (GBM) remains a lethal brain tumor due to therapy resistance. While autophagy contributes to temozolomide (TMZ) resistance, its regulation is incompletely understood. This study investigates the role of replication factor RFC4, which is associated with poor prognosis and TMZ resistance in GBM. Multi-omics analyses and molecular experiments reveal that TMZ-induced chromatin accessibility enables transcription factor YY1 to bind the RFC4 promoter and upregulate its expression. RFC4, in turn, stabilizes the kinase STK38, which is essential for autophagosome formation. The RFC4-STK38 interaction facilitates BECN1 recruitment, thereby activating autophagy. Phosphorylation of STK38 at T444 stabilizes this complex, whereas a phospho-deficient mutant impairs autophagy. In vivo, RFC4 overexpression confers TMZ resistance, reversible by autophagy inhibition. Thus, our findings identify the RFC4-STK38-BECN1 axis as a mechanism underlying TMZ resistance and a potential target for precision therapy in GBM.
PMID:41872171 | DOI:10.1038/s41467-026-70798-1