SNORD42A serves as an oncogenic biomarker in non-small cell lung cancer.
7 affiliations
- 1Pudong Gongli Hospital, Shanghai University of Medicine & Health Sciences, Shanghai, China.
- 2Basic Medical College, Shanghai University of Medicine & Health Sciences, Shanghai, China.
- 3Department of Geriatrics, Huashan Hospital, Fudan University, Shanghai, China.
- 4Department of Clinical Laboratory Medicine, Shanghai Tenth People's Hospital of Tongji University, Shanghai, China.
- 5Department of Thoracic Surgery, Haiyang People's Hospital, Haiyang, China.
- 6Shanghai University of Traditional Chinese Medicine, Shanghai, China.
- 7Clinical Genetics Center, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Abstract
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. 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. 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. 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.
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BibTeX
@article{cui2026snord42a,
title = {{SNORD42A serves as an oncogenic biomarker in non-small cell lung cancer.}},
author = {Chunhong Cui and Yan Wang and Jing Xia and Tengfei Sun and Yuwei Chen and Hui Wang and Qi Wu},
journal = {Journal of thoracic disease},
year = {2026},
month = oct,
doi = {10.21037/jtd-2026-2284},
url = {https://europepmc.org/article/MED/42996944},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - SNORD42A serves as an oncogenic biomarker in non-small cell lung cancer.
AU - Chunhong Cui
AU - Yan Wang
AU - Jing Xia
AU - Tengfei Sun
AU - Yuwei Chen
AU - Hui Wang
AU - Qi Wu
PY - 2026
DA - 2026/10/22
JO - Journal of thoracic disease
DO - 10.21037/jtd-2026-2284
UR - https://europepmc.org/article/MED/42996944
AB - 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. 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. 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. 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.
SN - 2072-1439
SN - 2077-6624
ER -