ArticleClinical & experimental metastasis1996
An in vitro invasion model for human renal cell carcinoma cell lines mimicking their metastatic abilities.
Article in Clinical & experimental metastasis, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Papillary renal cell carcinoma: a clinicopathological and whole-genome exon sequencing study.International journal of clinical and experimental pathology · 2015Article
- A novel assay for the quantification of invasion from raft cultures of lung carcinomas.Clinical & experimental metastasis · 2004Article
- The von Hippel-Lindau tumor suppressor gene inhibits hepatocyte growth factor/scatter factor-induced invasion and branching morphogenesis in renal carcinoma cells.Molecular and cellular biology · 1999Article
- Alterative expression of the collagenase and adhesion molecules in the highly metastatic clones of human colonic cancer cell lines.Clinical & experimental metastasis · 1998Article
- Nitric oxide induced by tumor cells activates tumor cell adhesion to endothelial cells and permeability of the endothelium in vitro.Clinical & experimental metastasis · 1997Article
- All-trans-retinoic acid-dependent inhibition of E-cadherin-based cell adhesion with concomitant dephosphorylation of beta-catenin in metastatic human renal carcinoma cells.Japanese journal of cancer research : Gann · 1997Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We developed a modified in vitro invasion assay system using monolayers of vascular endothelial cells. A type I collagen gel was formed in plastic dishes, and overlaid with type IV collagen. Calf pulmonary arterial endothelial (CPAE) cells were seeded onto these plates, and incubated until they reached confluence. Five human renal cell carcinoma cell lines with various metastatic potentials in vivo were then seeded on the monolayer CPAE cells, and their colony formation and invasion activities were examined for 9 days. At day 4, the highly metastatic cell lines increased the number of colony foci on monolayer CPAE cells several fold higher than their poorly metastatic counterpart. The horizontal spreading patterns were also different between poorly and highly metastatic cell lines. On day 9, the number of carcinoma foci that penetrated the monolayer of CPAE cells and type IV collagen sheets into type I collagen gels in highly metastatic cell lines greatly increased as compared with that of poorly metastatic cell lines. Our in vitro invasion assay using monolayer CPAE cells would be useful to evaluate protease activities and colony formation during invasion.
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