ArticleCell death and differentiation2026
SNORA23-KDM5C epigenetic axis mediates dual DNA repair pathways to drive radioresistance in esophageal squamous cell carcinoma.
Article in Cell death and differentiation, 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
Radioresistance remains a major barrier in esophageal squamous cell carcinoma (ESCC). This study demonstrates small nucleolar RNA SNORA23 as a pathogenic epigenetic driver of intrinsic radioresistance, with its overexpression tightly correlating with advanced T-stage, lymph node metastasis, and adverse clinical outcomes in a chemoradiotherapy cohort. Mechanistically, SNORA23 directly binds the ARID domain of histone demethylase KDM5C via a structurally defined G11-Ser169 interface-obstructing KDM5C chromatin binding to derepress DNA repair scaffolding gene SFPQ. This chromatin reprogramming enables SFPQ-facilitated recruitment of RAD51 and Ku80 to DNA double-strand breaks, accelerating homologous recombination (HR) and non-homologous end joining (NHEJ). SFPQ high expression recapitulates SNORA23-mediated repair enhancement and reduced radiosensitivity. Therapeutically, SNORA23-targeting antisense oligonucleotides (ASOs) disrupt this axis, impair DNA repair, and synergize with radiotherapy to suppress tumor growth and prolong survival in vivo without evident systemic toxicity These findings define a snoRNA-chromatin-repair axis driving therapeutic resistance and support SNORA23 inhibition as a promising strategy to overcome radioresistance in ESCC.
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Registered trials
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