ArticlePancreas2010
Divalent cations modulate alpha2beta1 integrin-mediated malignancy in a novel 3-dimensional in vitro model of pancreatic cancer.
Article in Pancreas, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 4 citations in OpenAlex.
- A 3D matrix platform for the rapid generation of therapeutic anti-human carcinoma monoclonal antibodies.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
objectivesWe previously showed that divalent cations regulate alpha2beta1 integrin-mediated pancreatic cancer cell interactions with type I collagen in 2 dimensions (2D), including cell adhesion, migration, and proliferation. Presently, we examined divalent cation-dependent alpha2beta1 integrin-mediated pancreatic cancer cell adhesion and proliferation on type I collagen in a novel 3D in vitro model.
methodsCell attachment, proliferation, and antibody inhibition assays on type I collagen in both 2D and 3D, and microscopy and immunoblotting were used for these studies.
resultsAs in 2D, cell attachment on type I collagen in 3D is Mg-dependent and inhibited by Ca. Proliferation in 3D is also Mg-dependent, but maximal when Mg is present at concentrations that promote maximal cell adhesion and Ca is present at concentrations less than Mg. Immunoblotting studies demonstrate that the divalent cation-dependent changes in cell-cell adhesion observed on type I collagen in both 2D and 3D are associated with the changes in E-cadherin and beta-catenin expression. Antibody inhibition assays indicate further that the alpha2beta1 integrin specifically mediates proliferation on type I collagen in 3D under altered divalent cation conditions.
conclusionsDivalent cation shifts could activate alpha2beta1 integrin-mediated malignancy in the type I collagen-rich 3D tumor microenvironment of pancreatic 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.