ArticleTranslational lung cancer research2025
Article in Translational lung cancer research, 2025. 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: Lung adenocarcinoma (LUAD), the predominant histological subtype of non-small cell lung cancer, remains a leading cause of cancer-related mortality worldwide. Suppressor of fused (SuFu) protein, a key negative regulator of the Hedgehog (Hh) signaling pathway, exhibits context-dependent roles in cancer, functioning variably as an oncogene or tumor suppressor. While loss-of-function mutations in SuFu have been implicated in tumorigenesis across several cancer types, their clinical significance in LUAD remains unclear. The study aimed to explore SuFu's regulatory effects in LUAD and evaluate its clinical value as a biomarker. Methods: Endogenous molecular data of SuFu in LUAD were obtained from public bioinformatics databases to investigate SuFu's impact on tumor mutational burden (TMB) and survival. Additionally, immunohistochemical staining was performed to analyze SuFu's impact on clinical features and overall survival (OS). SuFu was knocked out in A549 cells, followed by transcriptome sequencing and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. Three mutant (MT) SuFu vectors were constructed. Dual-luciferase assays and Co-immunoprecipitation (Co-IP) experiments were conducted using these vectors to explore the functional interaction between SuFu and Glioma-associated oncogene homolog 1 (Gli1). Overexpressing cell lines of MT SuFu were established in H1975, and the transcription level of Gli1 was detected by real-time quantitative polymerase-chain reaction (RT-qPCR). Overexpressing cell lines of wild type (WT) SuFu were established in A549 and H1975, and the regulatory effect of WT SuFu on the growth of LUAD was verified through functional experiments Results: The bioinformatics analysis results indicated that SuFu was negatively correlated with TMB in LUAD, while the latter was positively correlated with high-grade node stage (N stage) and higher overall stage. In addition, high expression of SuFu significantly improved the prognosis of LUAD patients, while Conclusions: SuFu's rare somatic mutations (~1%) had clinical value and were confirmed as markers of LUAD progression, providing new insights into the pathogenesis of LUAD. Potential therapeutic strategies involving the SuFu-Gli1 axis have also been proposed for precision medicine in the treatment of LUAD.
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