ArticleCancer genomics & proteomics
Microarray-based Analysis of Genes, Transcription Factors, and Epigenetic Modifications in Lung Cancer Exposed to Nitric Oxide.
Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 21 citations in OpenAlex.
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- Preliminary Study on the Expression of CLLD7 and CHC1L Proteins in Oral Squamous Cell Carcinoma.European journal of dentistry · 2024Article
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- Engineering siRNA-loaded and RGDfC-targeted selenium nanoparticles for highly efficient silencing of DCBLD2 gene for colorectal cancer treatment.Discover nano · 2023Article
- MRPL51 is a downstream target of FOXM1 in promoting the malignant behaviors of lung adenocarcinoma.Oncology letters · 2023Article
- A Rab-bit hole: Rab40 GTPases as new regulators of the actin cytoskeleton and cell migration.Frontiers in cell and developmental biology · 2023Review
- Gasotransmitters in the tumor microenvironment: Impacts on cancer chemotherapy (Review).Molecular medicine reports · 2022Review
- Aberrant mitochondrial homeostasis at the crossroad of musculoskeletal ageing and non-small cell lung cancer.PloS one · 2022Article
- Pillars and Gaps of S-Nitrosylation-Dependent Epigenetic Regulation in Physiology and Cancer.Life (Basel, Switzerland) · 2021Review
- GRPEL2 Knockdown Exerts Redox Regulation in Glioblastoma.International journal of molecular sciences · 2021Article
- Lipid raft-disrupting miltefosine preferentially induces the death of colorectal cancer stem-like cells.Clinical and translational medicine · 2021Article
- Abnormal Expression of Mitochondrial Ribosomal Proteins and Their Encoding Genes with Cell Apoptosis and Diseases.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimNitric oxide (NO) is recognized as an important biological mediator that exerts several human physiological functions. As its nature is an aqueous soluble gas that can diffuse through cells and tissues, NO can affect cell signaling, the phenotype of cancer and modify surrounding cells. The variety of effects of NO on cancer cell biology has convinced researchers to determine the defined mechanisms of these effects and how to control this mediator for a better understanding as well as for therapeutic gain. MATERIALS AND
methodsWe used bioinformatics and pharmacological experiments to elucidate the potential regulation and underlying mechanisms of NO in non-small a lung cancer cell model.
resultsUsing microarrays, we identified a total of 151 NO-regulated genes (80 up-regulated genes, 71 down-regulated genes) with a strong statistically significant difference compared to untreated controls. Among these, the genes activated by a factor of more than five times were: DCBLD2, MGC24975, RAB40AL, PER3, RCN1, MRPL51, PTTG1, KLF5, NFIX. On the other hand, the expression of RBMS2, PDP2, RBAK, ORMDL2, GRPEL2, ZNF514, MTHFD2, POLR2D, RCBTB1, JOSD1, RPS27, GPR4 genes were significantly decreased by a factor of more than five times. Bioinformatics further revealed that NO exposure of lung cancer cells resulted in a change in transcription factors (TFs) and epigenetic modifications (histone modification and miRNA). Interestingly, NO treatment was shown to potentiate cancer stem cell-related genes and transcription factors Oct4, Klf4, and Myc.
conclusionThrough this comprehensive approach, the present study illustrated the scheme of how NO affects molecular events in lung cancer cells.
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