ArticleiScience2026
UHRF1 drives subtype-independent aggressiveness and immune evasion in small cell lung cancer through PRC2 interactions.
Article in iScience, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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7 authors.
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Abstract
Small cell lung cancer (SCLC) is an aggressive neuroendocrine (NE) carcinoma characterized by early metastasis and an immune-cold microenvironment. We show that UHRF1, a chromatin-associated effector of RB1/E2F signaling, promotes SCLC growth and metastasis across major molecular subtypes. Using human SCLC cell lines, orthotopic and intracardiac xenografts, and genetically engineered mouse models, we found that loss of UHRF1 reduces proliferation, invasion, tumor burden, and metastasis while reprogramming tumors away from NE states toward an inflamed transcriptional program. UHRF1-deficient tumors upregulate chemokines and exhibit increased infiltration of CD8
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