ArticleMolecular cancer research : MCR2010
ASCL1 regulates the expression of the CHRNA5/A3/B4 lung cancer susceptibility locus.
Article in Molecular cancer research : MCR, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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
16 citing papers in PubMed, 32 citations in OpenAlex.
- Integrative genomic profiling reveals characteristics of lymph node metastasis in small cell lung cancer.Translational lung cancer research · 2023Article
- α9-Containing Nicotinic Receptors in Cancer.Frontiers in cellular neuroscience · 2021Review
- Cervical Cancer Correlates with the Differential Expression of Nicotinic Acetylcholine Receptors and Reveals Therapeutic Targets.Marine drugs · 2019Article
- Chronic Menthol Does Not Change Stoichiometry or Functional Plasma Membrane Levels of MouseMolecular pharmacology · 2019Article
- Proteins and chemical chaperones involved in neuronal nicotinic receptor expression and function: an update.British journal of pharmacology · 2018Review
- Expression patterns for nicotinic acetylcholine receptor subunit genes in smoking-related lung cancers.Oncotarget · 2017Article
- Nicotinic cholinergic receptors in esophagus: Early alteration during carcinogenesis and prognostic value.World journal of gastroenterology · 2016Article
- NeuroD1 mediates nicotine-induced migration and invasion via regulation of the nicotinic acetylcholine receptor subunits in a subset of neural and neuroendocrine carcinomas.Molecular biology of the cell · 2014Article
- Association between a 15q25 gene variant, nicotine-related habits, lung cancer and COPD among 56,307 individuals from the HUNT study in Norway.European journal of human genetics : EJHG · 2013Article
- Nicotine-modulated subunit stoichiometry affects stability and trafficking of α3β4 nicotinic receptor.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Epigenetic screen identifies genotype-specific promoter DNA methylation and oncogenic potential of CHRNB4.Oncogene · 2013Article
- Nicotinic acetylcholine receptors mediate lung cancer growth.Frontiers in physiology · 2013Article
- Alternative CHRNB4 3'-UTRs mediate the allelic effects of SNP rs1948 on gene expression.PloS one · 2013Article
- Nicotinic α5 receptor subunit mRNA expression is associated with distant 5' upstream polymorphisms.European journal of human genetics : EJHG · 2011Article
- The nicotinic acetylcholine receptor CHRNA5/A3/B4 gene cluster: dual role in nicotine addiction and lung cancer.Progress in neurobiology · 2010Review
- From smoking to lung cancer: the CHRNA5/A3/B4 connection.Oncogene · 2010Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Tobacco contains a variety of carcinogens as well as the addictive compound nicotine. Nicotine addiction begins with the binding of nicotine to its cognate receptor, the nicotinic acetylcholine receptor (nAChR). Genome-wide association studies have implicated the nAChR gene cluster, CHRNA5/A3/B4, in nicotine addiction and lung cancer susceptibility. To further delineate the role of this gene cluster in lung cancer, we examined the expression levels of these three genes as well as other members of the nAChR gene family in lung cancer cell lines and patient samples using quantitative reverse transcription-PCR. Overexpression of the clustered nAChR genes was observed in small-cell lung carcinoma (SCLC), an aggressive form of lung cancer highly associated with cigarette smoking. The overexpression of the genomically clustered genes in SCLC suggests their coordinate regulation. In silico analysis of the promoter regions of these genes revealed putative binding sites in all three promoters for achaete-scute complex homolog 1 (ASCL1), a transcription factor implicated in the pathogenesis of SCLC, raising the possibility that this factor may regulate the expression of the clustered nAChR genes. Consistent with this idea, knockdown of ASCL1 in SCLC, but not in non-SCLC, led to a significant decrease in expression of the alpha 3 and beta 4 genes without having an effect on any other highly expressed nAChR gene. Our data indicate a specific role for ASCL1 in regulating the expression of the CHRNA5/A3/B4 lung cancer susceptibility locus. This regulation may contribute to the predicted role that ASCL1 plays in SCLC tumorigenesis.
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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.