ArticleCells2020
Carbonic Anhydrase III Promotes Cell Migration and Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma.
Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- Proteomic identification and histopathological validation of candidate biomarkers CA1, HBB, Torsin A, andFrontiers in medicine · 2026Article
- Carbonic Anhydrase Inhibitors in Oncology.Sub-cellular biochemistry · 2026Review
- Carbonic Anhydrase 3 Overexpression Modulates Signalling Pathways Associated with Cellular Stress Resilience and Proteostasis.International journal of molecular sciences · 2025Article
- The reducing effect of TNF-α on carbonic anhydrase III gene expression in colon carcinoma and osteosarcoma cells.Cytotechnology · 2025Article
- SERPINB6 Promotes Epithelial-Mesenchymal Transition via PI3K/AKT/mTOR Signalling Pathway in Glioma.Journal of cellular and molecular medicine · 2025Article
- The development of a high-plex spatial proteomic methodology for the characterisation of the head and neck tumour microenvironment.NPJ precision oncology · 2025Article
- Increased V-ATPase activity can lead to chemo-resistance in oral squamous cell carcinoma via autophagy induction: new insights.Medical oncology (Northwood, London, England) · 2024Review
- Carbonic Anhydrase 3 is required for cardiac repair post myocardial infarction via Smad7-Smad2/3 signaling pathway.International journal of biological sciences · 2024Article
- Discovery of the first-in-class potent and isoform-selective human carbonic anhydrase III inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2023Article
- Carbonic anhydrases III and IX are new players in the crosstalk between adrenocortical carcinoma and its altered adipose microenvironment.Journal of endocrinological investigation · 2023Article
- Impact of tissue inhibitor of metalloproteinases-3 genetic variants on clinicopathological characteristics of urothelial cell carcinoma.Journal of Cancer · 2023Article
- MicroRNA Let-7a, -7e and -133a Attenuate Hypoxia-Induced Atrial Fibrosis via Targeting Collagen Expression and the JNK Pathway in HL1 Cardiomyocytes.International journal of molecular sciences · 2022Article
- The impact ofAging · 2022Article
- Interleukin-6 and Interleukin-8 Regulate STAT3 Activation Migration/Invasion and EMT in Chrysophanol-Treated Oral Cancer Cell Lines.Life (Basel, Switzerland) · 2021Article
- A review of gliomas-related proteins. Characteristics of potential biomarkers.American journal of cancer research · 2021Review
- Targeting the pH Paradigm at the Bedside: A Practical Approach.International journal of molecular sciences · 2020Review
- Silencing PROK2 Inhibits Invasion of Human Cervical Cancer Cells by Targeting MMP15 Expression.International journal of molecular sciences · 2020Article
- SCAP Mediated GDF15-Induced Invasion and EMT of Esophageal Cancer.Frontiers in oncology · 2020Article
Corrections and comments
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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
Epithelial-mesenchymal transition (EMT) is strongly correlated with tumor metastasis and contains several protein markers, such as E-cadherin. Carbonic anhydrase III (CA III) exhibits low carbon dioxide hydratase activity in cancer. However, the detailed mechanisms of CA III and their roles in oral cancer are still unknown. This study established a CA III-overexpressed stable clone and observed the expression of CA III protein in human SCC-9 and SAS oral cancer cell lines. The migration and invasion abilities were determined using a Boyden chamber assay. Our results showed that the overexpression of CA III protein significantly increased the migration and invasion abilities in oral cancer cells. Moreover, a whole genome array analysis revealed that CA III regulated epithelial-mesenchymal transition by reducing the expression of epithelial markers. Data from the GEO database also demonstrated that CA III mRNA is negatively correlated with CDH1 mRNA. Mechanistically, CA III increased the cell motility of oral cancer cells through the FAK/Src signaling pathway. In conclusion, this suggests that CA III promotes EMT and cell migration and is potentially related to the FAK/Src signaling pathway in oral cancer.
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Registered trials
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.