ArticleFrontiers in oncology2026
SPRTN preserves RNA polymerase I transcription under genotoxic drug stress in lung adenocarcinoma.
Article in Frontiers in 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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Abstract
Background: Hyperactivated RNA polymerase I (Pol I)-driven ribosomal DNA (rDNA) transcription sustains malignant growth and chemotherapy tolerance in lung adenocarcinoma (LUAD). Genotoxic chemotherapeutics such as doxorubicin and cisplatin preferentially damage rDNA by inducing DNA-protein crosslinks (DPCs), yet how tumor cells preserve Pol I transcriptional output under this damage remains poorly understood. Methods: We investigated SPRTN function in LUAD using complementary approaches spanning molecular, cellular, and Results: SPRTN was enriched at the rDNA promoter, limited basal DPC accumulation, sustained Pol I transcriptional output, suppressed the p53-p21 nucleolar stress checkpoint, and promoted Pol I-dependent proliferation. Under doxorubicin or cisplatin treatment, SPRTN was recruited to G-quadruplex-rich rDNA promoters, a process associated with PARP-1 co-recruitment, and facilitated DPC resolution and transcriptional recovery. Catalytically inactive SPRTN failed to resolve rDNA-DPCs and restore Pol I output under both basal and drug-treated conditions. Doxorubicin- and cisplatin-resistant LUAD cells exhibited elevated SPRTN expression and enhanced rRNA synthesis relative to parental cells. SPRTN knockdown increased apoptotic response to doxorubicin and cisplatin, and co-inhibition of SPRTN and Pol I additively induced apoptosis in both parental and resistant cells. SPRTN further promoted Pol I-dependent migration and invasion. Transcriptomically, SPRTN was upregulated in LUAD, correlated with advanced disease stage and reduced overall survival, and was transcriptionally activated by ZEB1 and post-transcriptionally repressed by miR-195-5p. Conclusion: These findings establish SPRTN as an rDNA-associated repair factor that couples genotoxic damage resolution to Pol I transcriptional resilience, defining the SPRTN-Pol I axis as a determinant of nucleolar homeostasis and therapeutic vulnerability in lung adenocarcinoma.
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