ArticleCancer cell international2018
CLDN2 inhibits the metastasis of osteosarcoma cells via down-regulating the afadin/ERK signaling pathway.
Article in Cancer cell international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- Dynamic remodeling of the KRAS interactome by direct RAS inhibitors with distinct mechanism of action reveals convergent responses.Oncogene · 2026Article
- The PRKN/METTL3/CLDN2 axis promotes colorectal cancer development through epigenetic mechanisms.Cell biology and toxicology · 2026Article
- CRISPR/Cas9-mediated claudin-2 knockout in HCT116 cells reveals its key role in colorectal cancer progression.Oncology letters · 2026Article
- The directionality of collective cell delamination is governed by tissue architecture and cell adhesion in aiScience · 2025Article
- Identification of claudin-2 as a promising biomarker for early diagnosis of pre-diabetes.Frontiers in pharmacology · 2024Article
- Expression patterns of claudins in cancer.Heliyon · 2023Review
- Multidirectional characterization of cellular composition and spatial architecture in human multiple primary lung cancers.Cell death & disease · 2023Article
- Review
- The role and mechanism of claudins in cancer.Frontiers in oncology · 2022Review
- miR-1270 enhances the proliferation, migration, and invasion of osteosarcoma <em>via</em> targeting cingulin.European journal of histochemistry : EJH · 2021Article
- Claudin-2 promotes colorectal cancer liver metastasis and is a biomarker of the replacement type growth pattern.Communications biology · 2021Article
- LncRNA EBLN3P promotes the progression of osteosarcoma through modifying the miR-224-5p/Rab10 signaling axis.Scientific reports · 2021Article
- Pre-mRNA processing factor 3 enhances the progression of keratinocyte-derived cutaneous squamous cell carcinoma by regulating the JAK2/STAT3 pathway.Scientific reports · 2020Article
- C-terminal of E1A binding protein 2 promotes the malignancy of osteosarcoma cells via JAK1/Stat3 signaling.Journal of cell communication and signaling · 2020Article
- LncRNA NEAT1 Promotes the Progression of Gastric Cancer Through Modifying the miR-1224-5p/RSF1 Signaling Axis.Cancer management and research · 2020Article
- Expression of Carboxypeptidase X M14 Family Member 2 Accelerates the Progression of Hepatocellular Carcinoma via Regulation of the gp130/JAK2/Stat1 Pathway.Cancer management and research · 2020Article
- Pre-mRNA Processing Factor 8 Accelerates the Progression of Hepatocellular Carcinoma by Regulating the PI3K/Akt Pathway.OncoTargets and therapy · 2020Article
- Long Noncoding RNACancer management and research · 2020Article
- Role of Claudin Proteins in Regulating Cancer Stem Cells and Chemoresistance-Potential Implication in Disease Prognosis and Therapy.International journal of molecular sciences · 2019Review
- C-Terminus of E1A Binding Protein 1 Stimulates Malignant Phenotype in Human Hepatocellular Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn an earlier study, we investigated the expression of tight junction protein claudins (CLDNs) in human osteosarcoma (OS) cells, and the CLDN2 was found to be down-regulated in primary tumor cells compared with normal osteoblast cells. Here, we sought to explore the effects of CLDN2 on the malignant phenotype of OS and the underlying molecular mechanisms.
methodsThe expression patterns of CLDN2 and afadin in OS tissues and histologically non-neoplastic bone tissues were explored via immunohistochemistry and western blotting. CLDN2 expression levels in an OS cell line stably expressing CLDN2 and an osteoblast cell line with a CLDN2 knockout were confirmed by western blotting and immunofluorescence staining. The malignant phenotype of OS cells and osteoblast cells in vitro was assessed using a cell counting kit-8 assay, transwell assay and wound-healing experiment. Western blotting was utilized to detect the activation state of Ras/Raf/MEK/ERK pathway. Moreover, an RNA interference method were used to silence afadin in CLDN2-expressing OS cells.
resultsOur research group found that CLDN2 and afadin was underexpressed in OS tissues, and the overexpression of CLDN2 significantly inhibited the migration abilities of OS cells. Genetic silencing of afadin in CLDN2-overexpressing OS cells promoted U2OS cell motility and activation of the Ras/Raf/MEK/ERK pathway.
conclusionsIn this study, we confirmed that CLDN2 expression significantly inhibited the malignant phenotype of OS cells in vitro. Inhibition of the ERK pathway by afadin may be one of the mechanisms by which CLDN2 blocks the metastasis phenotype of OS cells.
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