Claudia Andl
Faculty Member
Last active: 10/13/2015

Cathepsin B is the driving force of esophageal cell invasion in a fibroblast-dependent manner.

Andl CD, McCowan KM, Allison GL, Rustgi AK
Neoplasia. 2010 12 (6): 485-98

PMID: 20563251 · PMCID: PMC2887089 · DOI:10.1593/neo.10216

Esophageal cancer, which frequently exhibits coordinated loss of E-cadherin (Ecad) and transforming growth factor beta (TGFbeta) receptor II (TbetaRII), has a high mortality rate. In a three-dimensional organotypic culture model system, esophageal keratinocytes expressing dominant-negative mutant versions of both Ecad and TbetaRII (ECdnT) invade into the underlying matrix embedded with fibroblasts. We also find that cathepsin B induction is necessary for fibroblast-mediated invasion. Furthermore, the ECdnT cells in this physiological context activate fibroblasts through the secretion of TGFbeta1, which, in turn, is activated by cathepsin B. These results suggest that the interplay between the epithelial compartment and the surrounding microenvironment is crucial to invasion into the extracellular matrix.

MeSH Terms (27)

Blotting, Western Cadherins Carcinoma, Squamous Cell Cathepsin B Cell Adhesion Cell Movement Cell Proliferation Cells, Cultured Coculture Techniques Enzyme-Linked Immunosorbent Assay Epithelial Cells Esophageal Neoplasms Esophagus Fibroblasts Fluorescent Antibody Technique Humans Immunoenzyme Techniques Keratinocytes Neoplasm Invasiveness Organ Culture Techniques Protein-Serine-Threonine Kinases Receptor, Transforming Growth Factor-beta Type II Receptors, Transforming Growth Factor beta Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger Tissue Array Analysis Transforming Growth Factor beta1

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