ArticleAnnals of translational medicine2020
Cell adhesion molecule 2 (CADM2) promotes brain metastasis by inducing epithelial-mesenchymal transition (EMT) in human non-small cell lung cancer.
Article in Annals of translational medicine, 2020. 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, 23 citations in OpenAlex.
- Oncohistone inhibition reshapes tumor-microenvironment communication in Diffuse Midline Glioma (DMG).bioRxiv : the preprint server for biology · 2026Article
- Genome-wide association study of lung function decline using elastic-net regression: a prospective analysis in Korean cohort.Human genomics · 2025Article
- Genetic analysis in African ancestry populations reveals genetic contributors to lung cancer susceptibility.American journal of human genetics · 2025Article
- Selection Signature Analysis of Whole-Genome Sequences to Identify Genome Differences Between Selected and Unselected Holstein Cattle.Animals : an open access journal from MDPI · 2025Article
- Prognostic role and tumor-suppressive effects of CADM family members and the potential molecular mechanisms of CADM1 in neuroblastoma.Discover oncology · 2025Article
- Breaking boundaries: role of the brain barriers in metastatic process.Fluids and barriers of the CNS · 2025Review
- CADM2 participates in endometriosis development by influencing the epithelial-mesenchymal transition.Reproductive sciences (Thousand Oaks, Calif.) · 2024Article
- Study on Potential Differentially Expressed Genes in Idiopathic Pulmonary Fibrosis by Bioinformatics and Next-Generation Sequencing Data Analysis.Biomedicines · 2023Article
- Surfaceome Profiling of Cell Lines and Patient-Derived Xenografts Confirm FGFR4, NCAM1, CD276, and Highlight AGRL2, JAM3, and L1CAM as Surface Targets for Rhabdomyosarcoma.International journal of molecular sciences · 2023Article
- Liver fibrosis-derived exosomal miR-106a-5p facilitates the malignancy by targeting SAMD12 and CADM2 in hepatocellular carcinoma.PloS one · 2023Article
- MiR-17-5p Targets and Downregulates CADM2, Activating the Malignant Phenotypes of Colon Cancer Cells.Molecular biotechnology · 2022Article
- Genome-wide interrogation of structural variation reveals novel African-specific prostate cancer oncogenic drivers.Genome medicine · 2022Article
- Proteomics of autism and Alzheimer's mouse models reveal common alterations in mTOR signaling pathway.Translational psychiatry · 2021Article
- Article
- High expression of cell adhesion molecule 2 unfavorably impacts survival in non-small cell lung cancer patients with brain metastases.Journal of thoracic disease · 2021Article
- The Immune Microenvironment in Brain Metastases of Non-Small Cell Lung Cancer.Frontiers in oncology · 2021Review
- The RNA interactome in the Hallmarks of Cancer.Wiley interdisciplinary reviews. RNAReview
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTo investigate the effect of CADM2 on brain metastasis in non-small cell lung cancer (NSCLC).
methodsHuman transcriptome-wide microarray analysis was used to identify gene expression in lung tissue of NSCLC patients with or without brain metastasis, which indicated that CADM2 was significantly up-regulated. Quantitative real-time PCR (qRT-PCR) was used to confirm the CADM2 up-regulation further. SiRNA was used to knock down the expression of CADM2 in NSCLC cell lines and a Transwell assay was performed to determine the effects of CADM2 knockdown on cell migration and invasion. The expressions of Vimentin and E-cadherin were detected by western blot assay.
resultsThe result of microarray analysis and qRT-PCR showed that CADM2 was significantly up-regulated in NSCLC patients with brain metastasis than in those without brain metastasis. The result of the Transwell assay showed that the migration and invasion abilities of NSCLC cells were inhibited after CADM2 knockdown. Also, the expression of Vimentin was reduced while E-cadherin was increased, followed by CADM2 knockdown.
conclusionsThe results showed that CADM2 might promote brain metastasis by inducing epithelial-mesenchymal transition (EMT) in human NSCLC. We propose that CADM2 can be used as a novel molecular target for the prevention and treatment in NSCLC with brain metastasis patients.
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