ArticleMedical science monitor : international medical journal of experimental and clinical research2017
CLDN1 Increases Drug Resistance of Non-Small Cell Lung Cancer by Activating Autophagy via Up-Regulation of ULK1 Phosphorylation.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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36 citing papers in PubMed, 48 citations in OpenAlex.
- Circadian-immune-related gene signature for lung squamous cell carcinoma: machine learning and multi-omics analysis.Translational cancer research · 2026Article
- Claudins proteins in brain tumors: expression patterns and therapeutic target.Biochemia medica · 2026Review
- Genome-wide CRISPR screening identifiesOncology letters · 2026Article
- Claudin-1 Contributes to Gastrointestinal Stromal Tumors (GIST) Resistance to Imatinib Mesylate (IM) via Regulation of FGFR-Signaling.International journal of molecular sciences · 2025Article
- Identification of Common Cancer Antigens Useful for Specific Immunotherapies to Colorectal Cancer and Liver Metastases.International journal of molecular sciences · 2025Article
- Expression Profiles of Five Common Cancer Membrane Protein Antigens Collected for the Development of Cocktail CAR-T Cell Therapies Applicable to Most Solid Cancer Patients.International journal of molecular sciences · 2025Article
- Tight junctional protein family, Claudins in cancer and cancer metastasis.Frontiers in oncology · 2025Review
- Hyper-IgE Syndrome: A Case Report with Insights from Bioinformatics Analysis of Key Pathways and Genes.Infection and drug resistance · 2025Article
- CLDN6 induces chemoresistance through protective autophagy in breast cancer.International journal of biological sciences · 2025Article
- Micro RNA-175 TargetsGenes · 2024Article
- Key genes and molecular mechanisms related to Paclitaxel Resistance.Cancer cell international · 2024Review
- Claudins in Cancer: A Current and Future Therapeutic Target.International journal of molecular sciences · 2024Review
- Deciphering the role of claudins in lung cancer.Frontiers in oncology · 2024Review
- Claudin-1 interacts with EPHA2 to promote cancer stemness and chemoresistance in colorectal cancer.Cancer letters · 2023Article
- Expression patterns of claudins in cancer.Heliyon · 2023Review
- Downregulation of Claudin5 promotes malignant progression and radioresistance through Beclin1-mediated autophagy in esophageal squamous cell carcinoma.Journal of translational medicine · 2023Article
- Improving the response to oxaliplatin by targeting chemotherapy-induced CLDN1 in resistant metastatic colorectal cancer cells.Cell & bioscience · 2023Article
- Review
- Article
- MCancer science · 2022Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND The aim of this study was to investigate the expression of CLDN1 in non-small cell lung cancer (NSCLC) and its mechanism of action in cisplatin resistance. MATERIAL AND METHODS A total of 55 patients with NSCLC admitted to our hospital between October 2013 and October 2015 were included. NSCLC tissues and tumor-adjacent tissues (≥5 cm from tumor edge) were collected. Among the 55 patients, 37 had adenocarcinoma and 18 had squamous cell carcinoma. Quantitative real-time polymerase chain reaction was used to determine mRNA expression, and protein expression was examined using Western blotting. CCK-8 assay was used to determine cell proliferation and Transwell assay was used to detect migration and invasion of the cells. Confocal microscopy was used to observe autophagosomes. RESULTS Increased CLDN1 expression promoted the development and metastasis of NSCLC. CLDN1 expression in A549/CDDP cells was up-regulated at both transcriptional and translational levels. Reduced CLDN1 expression decreased the drug resistance, proliferation, migration, and invasion abilities of A549/CDDP cells. Decreased CLDN1 expression promoted the apoptosis of A549/CDDP cells. CLDN1 enhanced CDDP drug resistance of A549 cells by activating autophagy. CLDN1 promoted the autophagy of A549 cells by up-regulating the phosphorylation level of ULK1. CONCLUSIONS The present study demonstrates that expression of CLDN1 in NSCLC is up-regulated and it is correlated with clinicopathological features. CLDN1 activates autophagy through up-regulation of ULK1 phosphorylation and promotes drug resistance of NSCLC cells to CDDP.
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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.