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Cancer cell invasion and EMT marker expression: a three‐dimensional study of the human cancer–host interface
Author(s) -
Bronsert P,
EnderleAmmour K,
Bader M,
Timme S,
Kuehs M,
Csanadi A,
Kayser G,
Kohler I,
Bausch D,
Hoeppner J,
Hopt UT,
Keck T,
Stickeler E,
Passlick B,
Schilling O,
Reiss CP,
Vashist Y,
Brabletz T,
Berger J,
Lotz J,
Olesch J,
Werner M,
Wellner UF
Publication year - 2014
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.4416
Subject(s) - cancer , cancer cell , biology , metastasis , pathology , cell , epithelial–mesenchymal transition , budding , cancer research , cytoplasm , adenocarcinoma , microbiology and biotechnology , medicine , genetics
Cancer cell invasion takes place at the cancer–host interface and is a prerequisite for distant metastasis. The relationships between current biological and clinical concepts such as cell migration modes, tumour budding and epithelial–mesenchymal transition ( EMT ) remains unclear in several aspects, especially for the 'real' situation in human cancer. We developed a novel method that provides exact three‐dimensional ( 3D ) information on both microscopic morphology and gene expression, over a virtually unlimited spatial range, by reconstruction from serial immunostained tissue slices. Quantitative 3D assessment of tumour budding at the cancer–host interface in human pancreatic, colorectal, lung and breast adenocarcinoma suggests collective cell migration as the mechanism of cancer cell invasion, while single cancer cell migration seems to be virtually absent. Budding tumour cells display a shift towards spindle‐like as well as a rounded morphology. This is associated with decreased E‐cadherin staining intensity and a shift from membranous to cytoplasmic staining, as well as increased nuclear ZEB1 expression. Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.