ArticleCancer management and research2019
Chronic cadmium exposure aggravates malignant phenotypes of nasopharyngeal carcinoma by activating the Wnt/β-catenin signaling pathway via hypermethylation of the casein kinase 1α promoter.
Article in Cancer management and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 20 citations in OpenAlex.
- The efficacy of sap obtained fromVeterinarni medicina · 2026Article
- Epigenetics: the master switch of nasopharyngeal carcinoma invasion and metastasis.Frontiers in immunology · 2026Review
- Epigenetic regulation of the β-catenin pathway in cadmium-induced colorectal cancer progression and chemoresistance.Frontiers in cell and developmental biology · 2026Review
- Transcriptomics-based analysis of key genes and potential mechanism and therapeutic agents in cadmium-induced esophageal squamous cell carcinoma progression.Scientific reports · 2025Article
- Mechanisms of Heavy Metal Cadmium (Cd)-Induced Malignancy.Biological trace element research · 2025Review
- The dynamic face of cadmium-induced Carcinogenesis: Mechanisms, emerging trends, and future directions.Current research in toxicology · 2024Review
- Article
- SETD1A promotes the proliferation and glycolysis of nasopharyngeal carcinoma cells by activating the PI3K/Akt pathway.Open medicine (Warsaw, Poland) · 2022Article
- Environmental Cadmium Exposure Promotes the Development, Progression and Chemoradioresistance of Esophageal Squamous Cell Carcinoma.Frontiers in cell and developmental biology · 2022Article
- Review
- Chronic Exposure to Cadmium Induces Differential Methylation in Mice Spermatozoa.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Epimutational effects of electronic cigarettes.Environmental science and pollution research international · 2021Review
- Multiomics Landscape Uncovers the Molecular Mechanism of the Malignant Evolution of Lung Adenocarcinoma Cells to Chronic Low Dose Cadmium Exposure.Frontiers in oncology · 2021Article
- Glucose and lipid lowering effects of Enhydra fluctuans extract in cadmium treated normal and type-2 diabetic model rats.BMC complementary and alternative medicine · 2019Article
- Cadmium exposure upregulates SNAIL through miR-30 repression in human lung epithelial cells.Toxicology and applied pharmacology · 2019Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOur previous study has shown that cadmium (Cd) exposure is not only a risk factor for nasopharyngeal carcinoma (NPC), but also correlated with the clinical stage and lymph node metastasis. However, the underlying molecular events of Cd involved in NPC progression remain to be elucidated. PURPOSE: The objective of this study was to decipher how Cd impacts the malignant phenotypes of NPC cells.
methodsNPC cell lines CNE-1 and CNE-2 were continuously exposed with 1 μM Cd chloride for 10 weeks, designating as chronic Cd treated NPC cells (CCT-NPC). MTT assay, colony formation assay and xenograft tumor growth were used to assess cell viability in vitro and in vivo. Transwell assays were performed to detect cell invasion and migration. The protein levels of E-cadherin, N-cadherin, Vimentin as well as β-catenin and casein kinase 1α(CK1α) were measured by Western blot. Immunofluorescence staining was used to observe the distribution of filament actin (F-actin), β-catenin and CK1α. The mRNA levels of downstream target genes of β-catenin were detected by RT-PCR. Wnt/β-catenin signaling activity was assessed by TOPFlash/FOPFlash dual luciferase report system. MS-PCR was used to detect the methylation status of CK1α. Finally, the activation of Wnt/β-catenin pathway and cell biological properties were examined following treatment of CCT-NPC cells with 5-aza-2-deoxy-cytidine(5-aza-CdR).
resultsCCT-NPC cells showed an increase in cell proliferation, colony formation, invasion and migration compared to the parental cells. Cd also induced cytoskeleton reorganization and epithelial-to-mesenchymal transition. Upregulation and nuclear translocation of β-catenin and increased luciferase activity accompanied with transcription of downstream target genes were found in CCT-NPC cells. Treatment of CCT-CNE1 cells with 5-aza-CdR could reverse the hypermethylation of CK1α and attenuate the cell malignancy.
conclusionThese results support a role for chronic Cd exposure as a driving force for the malignant progression of NPC via epigenetic activation of the Wnt/β-catenin pathway.
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