ArticleCell death & disease2017
NPAS2 promotes cell survival of hepatocellular carcinoma by transactivating CDC25A.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.
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Who cites it
42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 103 citations in OpenAlex.
- Decoding the role of aberrant RNA alternative splicing in hepatocellular carcinoma: a comprehensive review.Journal of cancer research and clinical oncology · 2023Pooled it
- Low circadian clock genes expression in cancers: A meta-analysis of its association with clinicopathological features and prognosis.PloS one · 2020Pooled it
- Multi-Omics Landscape of Circadian Clock Dysregulation Across the Chronic Liver Disease Spectrum.International journal of molecular sciences · 2026Review
- Comprehensive analysis and therapeutic implications of prognostic value of circadian rhythm genes in hepatocellular carcinoma.Journal of physiology and biochemistry · 2026Article
- Temporal dynamics in cancer immunotherapy: the interplay between circadian rhythms, tumor microenvironment, and immune checkpoint blockade.Journal of the National Cancer Center · 2026Review
- Hepatocellular Carcinoma Around the Clock.Current oncology (Toronto, Ont.) · 2026Review
- Unique Sertoli cell adaptations support enhanced spermatogenesis in chickens.Journal of animal science and biotechnology · 2025Article
- Lipid Metabolism Related Gene ACSL3 as a Biomarker for Predicting Immunotherapy Outcomes in Lung Adenocarcinoma.Cancer research and treatment · 2025Article
- Circadian Gene NPAS2 Relieves Hypertrophic Scar Formation via CDC25A-Mediated Fibroblasts Activity.Journal of cellular and molecular medicine · 2025Article
- Decoding Multifaceted Roles of Sleep-Related Genes as Molecular Bridges in Chronic Disease Pathogenesis.International journal of molecular sciences · 2025Review
- The Common Hallmarks and Interconnected Pathways of Aging, Circadian Rhythms, and Cancer: Implications for Therapeutic Strategies.Research (Washington, D.C.) · 2025Review
- The Biological Clock of Liver Metabolism in Metabolic Dysfunction-Associated Steatohepatitis Progression to Hepatocellular Carcinoma.Biomedicines · 2024Review
- NPAS2 dampens chemo-sensitivity of lung adenocarcinoma cells by enhancing DNA damage repair.Cell death & disease · 2024Article
- Review
- High expression of the circadian clock gene NPAS2 is associated with progression and poor prognosis of gastric cancer: A single-center study.World journal of gastroenterology · 2023Article
- NPAS2 promotes aerobic glycolysis and tumor growth in prostate cancer through HIF-1A signaling.BMC cancer · 2023Article
- Cyclin A-CDK1 suppresses the expression of the CDK1 activator CDC25A to safeguard timely mitotic entry.The Journal of biological chemistry · 2023Article
- Bioinformatic analysis of genetic changes CLOCK, BMAL1, CRY1, CRY2, PER1, PER2, PER3, and NPAS2 proteins in HCC patients.Hepatology forum · 2023Article
- Near-infrared fluorescence imaging of hepatocellular carcinoma cells regulated by β-catenin signaling pathway.Frontiers in oncology · 2023Article
- SRSF10 stabilizes CDC25A by triggering exon 6 skipping to promote hepatocarcinogenesis.Journal of experimental & clinical cancer research : CR · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidences show that disruption of the circadian rhythm is associated with tumor initiation and progression. Neuronal PAS domain protein 2 (NPAS2), one of the core circadian molecules, has been proved to be a potential prognostic biomarker in colorectal and breast cancers. However, to date, the potential functional roles and molecular mechanisms by which NPAS2 affects cancer cell survival are greatly unclear, especially in hepatocellular carcinoma (HCC). We first investigated the expression of NPAS2 and its clinical significance in HCC. We then systematically explored the role of NPAS2 in HCC cell survival both in vitro and in vivo and the underlying mechanism. NPAS2 was frequently upregulated in HCC, which significantly facilitated cell survival both in vitro and in vivo mainly by promoting cell proliferation and inhibiting mitochondria-dependent intrinsic apoptosis, and thus contributed to poor prognosis of HCC patients. Mechanistically, the survival-promoting role of NPAS2 was mediated by transcriptional upregulation of the CDC25A phosphatase and subsequent dephosphorylation of CDK2/4/6 and Bcl-2, which induced cell proliferation and inhibited cell apoptosis in HCC, respectively. Moreover, BMAL1, another core clock transcription factor, was identified to heterodimerize with NPAS2 to bind to the E-box element in the promoter of CDC25A and be associated with the NPAS2-mediated tumor cell survival in HCC. Our findings demonstrate that NPAS2 has a critical role in HCC cell survival and tumor growth, which is mainly mediated by transcriptional upregulation of CDC25A. Thereby, NPAS2 may serve as a potential therapeutic target in HCC patients.
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