ArticleOncogene2017
Elevated hydrostatic pressure enhances the motility and enlarges the size of the lung cancer cells through aquaporin upregulation mediated by caveolin-1 and ERK1/2 signaling.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 47 citations in OpenAlex.
- Hydrostatic pressure activates HIF-1α via β-catenin to promote stemness in breast cancer cells.FEBS open bio · 2026Article
- Differential Transcriptomic and Adhesion Responses of Human Periodontal Ligament Cells to Cyclic and Static Hydrostatic Pressure.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Orchestrating movement: the role of Caveolin-1 in migration and metastasis.Molecular cancer · 2025Review
- S1P induces bleb-based T cell motility via S1PR1-dependent activation of RhoA and WNK1.bioRxiv : the preprint server for biology · 2025Article
- Biomechanics of the tumor extracellular matrix and regulatory T cells: regulatory mechanisms and potential therapeutic targets.Cell communication and signaling : CCS · 2025Review
- Caveolin-1 inhibits the proliferation and invasion of lung adenocarcinoma via EGFR degradation.Scientific reports · 2025Article
- Confinement controls the directional cell responses to fluid forces.Cell reports · 2024Article
- The impact of tumor microenvironment: unraveling the role of physical cues in breast cancer progression.Cancer metastasis reviews · 2024Review
- Toward innovative approaches for exploring the mechanically regulated tumor-immune microenvironment.APL bioengineering · 2024Review
- Important functions and molecular mechanisms of aquaporins family on respiratory diseases: potential translational values.Journal of Cancer · 2024Review
- Biophysics in tumor growth and progression: from single mechano-sensitive molecules to mechanomedicine.Oncogene · 2023Review
- Aquaporin-mediated dysregulation of cell migration in disease states.Cellular and molecular life sciences : CMLS · 2023Review
- Expression of aquaporin 1, 3 and 5 in colorectal carcinoma: correlation with clinicopathological characteristics and prognosis.Pathology oncology research : POR · 2023Article
- Aquaporins in Tumor.Advances in experimental medicine and biology · 2023Article
- Hydrostatic pressure as a driver of cell and tissue morphogenesis.Seminars in cell & developmental biology · 2022Review
- Microfluidic Determination of Distinct Membrane Transport Properties between Lung Adenocarcinoma Cells CL1-0 and CL1-5.Biosensors · 2022Article
- The biophysics of cancer: emerging insights from micro- and nanoscale tools.Advanced nanobiomed research · 2022Article
- The interplay between physical cues and mechanosensitive ion channels in cancer metastasis.Frontiers in cell and developmental biology · 2022Review
- Molecular cancer cell responses to solid compressive stress and interstitial fluid pressure.Cytoskeleton (Hoboken, N.J.) · 2021Review
- Tissue engineered platforms for studying primary and metastatic neoplasm behavior in bone.Journal of biomechanics · 2021Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanical characteristics presented in cancer microenvironment are known to have pivotal roles in cancer metastasis, which accounts for the leading cause of death from malignant tumors. However, while a uniformly distributed high interstitial fluid pressure (IFP) is a common feature in solid tumors, the effects of high IFP on the motility and invasiveness of cancer cells remain obscure. Using cell-culture devices that simulated increased IFP conditions by applying hydrostatic pressure (HP) ranging from 0 to 20 mm Hg to the cells, we found that the elevated HPs increased the migration speeds, invasiveness, cell volume, filopodial number and aquaporin-1 (AQP1), Snail and vinculin expression levels, as well as phosphorylation of caveolin-1 and extracellular signal-regulated kinase1/2 (ERK1/2), in the lung cancer cells CL1-5 and A549. The increases of migration speed and cell volume correlated temporally with the increase of AQP1 expression. The elevated HP-induced migration acceleration was hindered by AQP1 knockdown using small interfering RNA (siRNA) transfection. Inhibition of ERK1/2 phosphorylation using the mitogen-activated protein kinase kinase inhibitor PD98059 abrogated the elevated HP-induced AQP1 upregulation and migration acceleration in the cancer cells. Caveolin-1 knockdown by siRNA transfection attenuated the HP-induced, ERK1/2-depedent AQP1 upregulation and migration acceleration. Further biochemical studies revealed that the caveolin-1 activation-driven ERK1/2 signaling is mediated by Akt1/2 phosphorylation. By contrast, the elevated HPs had negligible effects on the migration speed and volume of normal bronchial epithelial cells. These results disclose a novel mechanism relating high IFP to the invasiveness of cancer cells and highlight potential targets to impede cancer spreading.
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