ArticleNucleic acids research2014
Non-metastatic 2 (NME2)-mediated suppression of lung cancer metastasis involves transcriptional regulation of key cell adhesion factor vinculin.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 50 citations in OpenAlex.
- Beyond miRNAs: exploratory profiling of PIWI-interacting RNAs and small nucleolar RNAs in non-small cell lung cancer-related malignant pleural effusions.Translational lung cancer research · 2026Article
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- Histidine Phosphorylation: Protein Kinases and Phosphatases.International journal of molecular sciences · 2024Review
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- Mechanisms of action of NME metastasis suppressors - a family affair.Cancer metastasis reviews · 2023Review
- Zebrafish in Lung Cancer Research.Cancers · 2023Review
- Elevated Serum Vinculin in Patients with HBV/HCV-Associated Liver Cirrhosis and Hepatocellular Carcinoma: A Pilot Study.Biologics : targets & therapy · 2023Article
- Cervical cancer-derived exosomal miR-663b promotes angiogenesis by inhibiting vinculin expression in vascular endothelial cells.Cancer cell international · 2021Article
- Requirement of transcription factor NME2 for the maintenance of the stemness of gastric cancer stem-like cells.Cell death & disease · 2021Article
- [Roles of Histidine Kinases and Histidine Phosphatases in Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2021Review
- Loss of the Metastasis Suppressor NME1, But Not of Its Highly Related Isoform NME2, Induces a Hybrid Epithelial-Mesenchymal State in Cancer Cells.International journal of molecular sciences · 2021Article
- Activation of Nm23-H1 to suppress breast cancer metastasis via redox regulation.Experimental & molecular medicine · 2021Review
- Identification of aberrantly methylated‑differentially expressed genes and gene ontology in prostate cancer.Molecular medicine reports · 2020Article
- Vinculin expression in non-small cell lung cancer.The Journal of international medical research · 2020Article
- Mechanistic Modeling of Gene Regulation and Metabolism Identifies Potential Targets for Hepatocellular Carcinoma.Frontiers in genetics · 2020Article
- Characterization of Nme5-Like Gene/Protein from the Red AlgaMarine drugs · 2019Article
- Inhibition of ZIP4 reverses epithelial-to-mesenchymal transition and enhances the radiosensitivity in human nasopharyngeal carcinoma cells.Cell death & disease · 2019Article
- Therapeutic Opportunities in Colorectal Cancer: Focus on Melatonin Antioncogenic Action.BioMed research international · 2019Review
- Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
Corrections and comments
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Authors and funding
22 authors at 9 institutions in 3 countries.
Funding
Abstract
Tumor metastasis refers to spread of a tumor from site of its origin to distant organs and causes majority of cancer deaths. Although >30 metastasis suppressor genes (MSGs) that negatively regulate metastasis have been identified so far, two issues are poorly understood: first, which MSGs oppose metastasis in a tumor type, and second, which molecular function of MSG controls metastasis. Herein, integrative analyses of tumor-transcriptomes (n=382), survival data (n=530) and lymph node metastases (n=100) in lung cancer patients identified non-metastatic 2 (NME2) as a key MSG from a pool of >30 metastasis suppressors. Subsequently, we generated a promoter-wide binding map for NME2 using chromatin immunoprecipitation with promoter microarrays (ChIP-chip), and transcriptome profiling. We discovered novel targets of NME2 which are involved in focal adhesion signaling. Importantly, we detected binding of NME2 in promoter of focal adhesion factor, vinculin. Reduced expression of NME2 led to enhanced transcription of vinculin. In comparison, NME1, a close homolog of NME2, did not bind to vinculin promoter nor regulate its expression. In line, enhanced metastasis of NME2-depleted lung cancer cells was found in zebrafish and nude mice tumor models. The metastatic potential of NME2-depleted cells was remarkably diminished upon selective RNA-i-mediated silencing of vinculin. Together, we demonstrate that reduced NME2 levels lead to transcriptional de-repression of vinculin and regulate lung cancer metastasis.
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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.