SNORD42A serves as an oncogenic biomarker in non-small cell lung cancer
Year: 2026
Type: article
Abstract: Background: Despite substantial advances in therapeutic strategies, non-small cell lung cancer (NSCLC) remains the leading cause of cancer-related death worldwide. The poor prognosis of NSCLC is largely due to the limited efficacy of existing clinical treatments and the lack of reliable and effective molecular therapeutic targets. Studies have shown that small nucleolar RNAs (snoRNAs) play pivotal regulatory roles in multiple pathological processes involved in tumor formation and malignant progression. However, the specific biological functions and underlying molecular mechanisms of individual snoRNAs in the occurrence and development of NSCLC remain largely unclear, highlighting the need for systematic exploration. Methods: A reanalysis of genome-scale clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 knockout screening data covering all annotated snoRNAs in NSCLC cell lines was performed. Colony formation assays confirmed the functional role of SNORD42A in NSCLC cells. A combined bioinformatic analysis of our internal sequencing data and public datasets further identified the molecular locus of SNORD42A in the pathogenesis of NSCLC. Results: Genome-wide screening identified SNORD42A as a key candidate snoRNA regulating NSCLC cell proliferation. Both the in-house snoRNA sequencing data and bioinformatics analysis of The Cancer Genome Atlas (TCGA) cohort demonstrated that SNORD42A was significantly overexpressed in clinical NSCLC tissues compared with paired adjacent normal lung tissues, indicating its potential oncogenic role in NSCLC. Functional validation experiments further demonstrated that SNORD42A knockdown markedly inhibited the clonogenic capacity of NSCLC cells. Moreover, an integrative bioinformatics analysis of TCGA data revealed that SNORD42A expression was closely correlated with cell cycle regulation and cellular senescence signaling pathways, and its expression level was significantly associated with the clinical prognosis of patients with NSCLC. Conclusions: SNORD42A functions as a pro-tumorigenic factor that promotes NSCLC progression, with its effects potentially linked to alterations in cellular protein synthesis. This study revealed the functional importance of SNORD42A in NSCLC malignancy, suggesting that SNORD42A may serve as a novel prognostic biomarker and a promising therapeutic target for the treatment of NSCLC.
Source: Journal of Thoracic Disease
Language: English
Subfield: Cancer Research
Domain: Life Sciences
Open Access status: diamond
OpenAlex ID: W7224120031