ArticlePflugers Archiv : European journal of physiology2014
Acidic priming enhances metastatic potential of cancer cells.
Article in Pflugers Archiv : European journal of physiology, 2014. 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.
- Article
- Role of the Dual-Specificity Phosphatase 6 (DUSP6) in the Activation of ERK1/2 Signaling by Hypoxia or Acidosis in Tumor Cells.Advances in experimental medicine and biology · 2026Article
- Review
- pH-regulated single cell migration.Pflugers Archiv : European journal of physiology · 2024Review
- The Role of microRNAs in Gene Expression and Signaling Response of Tumor Cells to an Acidic Environment.International journal of molecular sciences · 2023Article
- Modeling Gas Plasma-Tissue Interactions in 3D Collagen-Based Hydrogel Cancer Cell Cultures.Bioengineering (Basel, Switzerland) · 2023Article
- Article
- Cancer heterogeneity and metastasis: life at the edge.Clinical & experimental metastasis · 2022Review
- Normalizing Tumor Vasculature to Reduce Hypoxia, Enhance Perfusion, and Optimize Therapy Uptake.Cancers · 2021Review
- Impact of the acidic environment on gene expression and functional parameters of tumors in vitro and in vivo.Journal of experimental & clinical cancer research : CR · 2021Article
- Acid-sensing ion channel 1 (ASIC1) mediates weak acid-induced migration of human malignant glioma cells.American journal of cancer research · 2021Article
- The Role of MicroRNA Expression for Proliferation and Apoptosis of Tumor Cells: Impact of Hypoxia-Related Acidosis.Advances in experimental medicine and biology · 2021Article
- Functional Impact of Acidosis-Regulated MicroRNAs on the Migration and Adhesion of Tumor Cells.Advances in experimental medicine and biology · 2021Article
- Adaptation to chronic acidic extracellular pH elicits a sustained increase in lung cancer cell invasion and metastasis.Clinical & experimental metastasis · 2020Article
- Article
- Acid-induced autophagy protects human gastric cancer cells from apoptosis by activating Erk1/2 pathway.Translational cancer research · 2019Article
- Extracellular Acidosis Modulates the Expression of Epithelial-Mesenchymal Transition (EMT) Markers and Adhesion of Epithelial and Tumor Cells.Neoplasia (New York, N.Y.) · 2019Article
- Chromatin accessibility changes are associated with enhanced growth and liver metastasis capacity of acid-adapted colorectal cancer cells.Cell cycle (Georgetown, Tex.) · 2019Article
- Inhibition of Carbonic Anhydrase IX by Ureidosulfonamide Inhibitor U104 Reduces Prostate Cancer Cell Growth, But Does Not Modulate Daunorubicin or Cisplatin Cytotoxicity.Oncology research · 2018Article
- Tumor Acidosis and Hypoxia Differently Modulate the Inflammatory Program: Measurements In Vitro and In Vivo.Neoplasia (New York, N.Y.) · 2017Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic acidosis is a common feature of tumor microenvironment and may affect the phenotype of tumor cells, including invasive capacity and formation of metastases. We tested whether previous exposure to an acidic environment alters metastatic potential of two rat carcinoma cell lines in the animal model. In addition, we determined the effect of an acidic environment on motility and invasive capacity of AT-1 prostate carcinoma cells in culture. Exposure of tumor cells to an acidic environment (pH 6.6, 5 % CO2, 6 h) prior to tail vein injection in rats enhanced formation of lung metastases significantly. In culture, acidosis increased cellular motility of AT-1 cells. When the tumor cells were transferred back to pH 7.4, enhanced motility persisted for at least 3 h but vanished after longer periods (24 h), therefore presenting a "short-term memory effect." Although acidosis augmented phosphorylation of ERK1/2 and p38, and inhibition of ERK1/2 phosphorylation or of p38 kinase activity reduced basal motility at pH 7.4, acidosis-induced increase in motility was not dependent on ERK1/2 or p38 kinase. Src family kinases were not involved either. By contrast, scavenging reactive oxygen species (ROS), known to be increased in AT-1 cells under acidic conditions, blunted acidosis-induced motility increase. Our data indicate that tumor cells may acquire enhanced motility in an acidic micromilieu, at least in part due to enhanced ROS formation. Because enhanced motility persists for at least 3 h after leaving the acidic environment, this may promote metastasis formation, as observed in our in vivo model.
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