ArticleOncogene2004
Identification of SCN3B as a novel p53-inducible proapoptotic gene.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
41 citing papers in PubMed, 70 citations in OpenAlex.
- SCN3B is an Anti-breast Cancer Molecule with Migration Inhibition Effect.Biochemical genetics · 2026Article
- In silico and in vitro assessment of TP53, ATM, RAD51, and BAX genes in gastric cancer and their contribution to radiotherapy resistance.Hereditas · 2025Article
- A Novel Function of NaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Functional Investigations of p53 Acetylation Enabled by Heterobifunctional Molecules.ACS chemical biology · 2024Article
- Is the voltage-gated sodium channel β3 subunit (SCN3B) a biomarker for glioma?Functional & integrative genomics · 2024Article
- Genomic view of the origins of cell-mediated immunity.Immunogenetics · 2023Article
- Voltage-gated sodium channels: from roles and mechanisms in the metastatic cell behavior to clinical potential as therapeutic targets.Frontiers in pharmacology · 2023Review
- Network Preservation Analysis Reveals Dysregulated Synaptic Modules and Regulatory Hubs Shared Between Alzheimer's Disease and Temporal Lobe Epilepsy.Frontiers in genetics · 2022Article
- Polyunsaturated Fatty Acids Mediated Regulation of Membrane Biochemistry and Tumor Cell Membrane Integrity.Membranes · 2021Review
- Pharmacological and nutritional targeting of voltage-gated sodium channels in the treatment of cancers.iScience · 2021Review
- Exploring the Therapeutic Potential of Membrane Transport Proteins: Focus on Cancer and Chemoresistance.Cancers · 2020Review
- Sodium Channel NaScientific reports · 2019Article
- In Vivo Evidence for Voltage-Gated Sodium Channel Expression in Carcinomas and Potentiation of Metastasis.Cancers · 2019Review
- Emerging roles for multifunctional ion channel auxiliary subunits in cancer.Cell calcium · 2019Review
- Contribution of voltage-gated sodium channel β-subunits to cervical cancer cells metastatic behavior.Cancer cell international · 2019Article
- Detection of annexin A8 antibodies in serum of patients with antiphospholipid syndrome.Biochemia medica · 2018Article
- Voltage-Gated Sodium Channel β Subunits and Their Related Diseases.Handbook of experimental pharmacology · 2018Review
- Preserved SCN4B expression is an independent indicator of favorable recurrence-free survival in classical papillary thyroid cancer.PloS one · 2018Article
- Regulation of SCN3B/scn3b by Interleukin 2 (IL-2): IL-2 modulates SCN3B/scn3b transcript expression and increases sodium current in myocardial cells.BMC cardiovascular disorders · 2016Article
- Voltage-gated sodium channels and cancer: is excitability their primary role?Frontiers in pharmacology · 2015Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor suppressor p53 is a transcription factor that induces growth arrest and/or apoptosis in response to cellular stress. To identify novel p53-inducible genes, we compared the expression of genes in normal mouse embryo fibroblasts (MEFs) to p53-null cells by cDNA representational difference analysis. We report here that expression of endogenous sodium channel subunit beta 3 (SCN3B) is upregulated in mouse embryonic fibroblasts by DNA damage in a p53-dependent manner. In addition, we found that SCN3B levels are upregulated in human cancer cell lines by DNA damaging agents, as well as by overexpression of p53, but not significantly by p63 or p73. Furthermore, we identified two putative p53-binding sites upstream of the first exon (RE1) and in the third intron (RE2). The p53 protein can directly interact with the putative p53-binding sites in vivo, as assessed by chromatin immunoprecipitation. A reporter gene assay revealed that these two p53-binding sites are functional response elements. The SCN3B protein appears to be localized to the endoplasmic reticulum (ER). Introduction of the SCN3B gene into T98G and Saos2 cells potently suppressed colony formation. Furthermore, we found that adenovirus-mediated transfer of SCN3B induced apoptosis when combined with anticancer agents. The results presented here suggest that SCN3B mediates a p53-dependent apoptotic pathway and may be a candidate for gene therapy combined with anticancer drugs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.