ArticleOncotarget2017
Claudin-3 expression increases the malignant potential of lung adenocarcinoma cells: role of epidermal growth factor receptor activation.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Molecular profiling of breast cancer in native American women reveals distinct genomic and transcriptomic features.NPJ precision oncology · 2026Article
- Claudins in ovarian cancer: emerging biomarkers and therapeutic targets.Tissue barriers · 2026Review
- The research trends and hotspots of claudins in the field of cancer.Cell adhesion & migration · 2025Review
- Deciphering the role of claudins in lung cancer.Frontiers in oncology · 2024Review
- Expression and Targeted Application of Claudins Family in Hepatobiliary and Pancreatic Diseases.Journal of hepatocellular carcinoma · 2024Review
- Interplay between EGFR, E-cadherin, and PTP1B in epidermal homeostasis.Tissue barriers · 2023Review
- Article
- Application of C-Terminal Clostridium Perfringens Enterotoxin in Treatment of Brain Metastasis from Breast Cancer.Cancers · 2022Review
- Suppression of the malignancy of mammary tumor in mice model by inactivated preparation ofVeterinary research forum : an international quarterly journal · 2022Article
- Nrf2 Activation Protects Against Organic Dust and Hydrogen Sulfide Exposure Induced Epithelial Barrier Loss andFrontiers in cellular and infection microbiology · 2022Article
- The role and mechanism of claudins in cancer.Frontiers in oncology · 2022Review
- CITED4 enhances the metastatic potential of lung adenocarcinoma.Thoracic cancer · 2021Article
- The effects of PIKfyve inhibitor YM201636 on claudins and malignancy potential of nonsmall cell cancer cells.Turkish journal of biology = Turk biyoloji dergisi · 2021Article
- Molecular engineering of antibodies for site-specific conjugation to lipid polydopamine hybrid nanoparticles.Acta pharmaceutica Sinica. B · 2020Article
- ZDHHC12-mediated claudin-3Acta pharmaceutica Sinica. B · 2020Article
- Intracellular Fate and Impact on Gene Expression of Doxorubicin/Cyclodextrin-Graphene Nanomaterials at Sub-Toxic Concentration.International journal of molecular sciences · 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
- Identification of claudin‑1, ‑3, ‑7 and ‑8 as prognostic markers in human laryngeal carcinoma.Molecular medicine reports · 2019Article
- Claudin-3 Inhibits Lung Squamous Cell Carcinoma Cell Epithelial-mesenchymal Transition and Invasion via Suppression of the Wnt/β-catenin Signaling Pathway.International journal of medical sciences · 2018Article
- Tight Junction Proteins and Signaling Pathways in Cancer and Inflammation: A Functional Crosstalk.Frontiers in physiology · 2018Review
Corrections and comments
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Authors and funding
20 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Claudins are essential for the formation and maintenance of tight junctions (TJ). The altered expression of claudin proteins has been described in a variety of malignancies. However, the alteration of these proteins in lung adenocarcinoma (ADC) are poorly understood. Therefore, we report, based on the protein expression analysis of a total of 275 patient samples, that claudin-3 (CLDN3) expression is significantly increased in ADC tissues and is associated with cancer progression, correlating significantly with the poor survival of ADC patients (p=0.041&0.029). More importantly, forcing CLDN3 expression in ADC cells without endogenous CLDN3 expression resulted in significant increases in the cell proliferation, anchorage-dependent growth, migration and drug-resistance. In addition, epidermal growth factor (EGF) signaling pathway modulates the expression of claudins in a number of solid tumors. However, the mechanism of tight junction regulation by EGF in ADC remains unclear. To investigate this mechanisms, ADC cell lines were treated with EGF and its inhibitor. EGF unregulated CLDN3 expression via the MEK/ERK or PI3K/Akt signaling pathways and was required for the maintenance of baseline CLDN3 expression. Furthermore, downregulation of CLDN3 expression in ADC cell was found to prevent the EGF-induced increase in cell proliferation. In conclusion, our results demonstrate a novel role of CLDN3 overexpression in promoting the malignant potential of lung adenocarcinoma. This function is potentially regulated by the EGF-activated MEK/ERK and PI3K-Akt pathways.
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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.