PMID- 10506935
OWN - NLM
STAT- MEDLINE
DCOM- 19991126
LR  - 20180607
IS  - 0213-3911 (Print)
IS  - 0213-3911 (Linking)
VI  - 14
IP  - 4
DP  - 1999 Oct
TI  - Cohort migration of carcinoma cells: differentiated colorectal carcinoma cells 
      move as coherent cell clusters or sheets.
PG  - 1183-97
LID - 10.14670/HH-14.1183 [doi]
AB  - Active migration of tumor cells is usually assessed as single cell locomotion in 
      vitro using Boyden chamber-type assays. In vivo, however, carcinoma cells, 
      malignant cells of epithelial origin, frequently invade the surrounding tissue as 
      coherent clusters or nests of cells. We have called this type of movement "cohort 
      migration". In our work, the invasion front of colon carcinomas consisted of 
      compact tumor glands, partially resolved glands or markedly resolved glands with 
      scattered tumor cell clusters or single cells lying ahead. In the former two 
      types, which constituted about a half of all cases, cohort migration seems to be 
      the predominant mechanism, whereas both cohort migration and single cell 
      locomotion may be involved in the last one. In this light, it is very 
      advantageous to investigate the mechanisms involved in the cohort migration. In 
      this review, we present a two-dimensional motility assay as a cohort migration 
      model, in which human colorectal carcinoma cells move outwards from the cell 
      islands mainly as localized coherent sheets of cells when stimulated with 
      12-O-tetradecanoylphorbol-13-acetate (TPA) or hepatocyte growth factor/scatter 
      factor (HGF/SF). Within the migrating cell sheets, wide intercellular gaps occur 
      at the lower portion of the cells to allow the cells to extend leading lamellae 
      forward while close cell-cell contacts remain at the upper portion of the cells. 
      This localized modulation of cell-cell adhesion at the lower portion of the cells 
      is associated with increased tyrosine phosphorylation of the E-cadherin-catenin 
      complex in TPA-induced cohort migration and with reduced alpha-catenin complexed 
      with E-cadherin in HGF/SF-induced cohort migration. Furthermore, fibronectin 
      deposited by migrating cells is essential for their movement, and on the 
      gelatin-coated substrate even degradation and remodeling of the substrate by 
      matrix metalloproteinases are also needed. Thus, in cohort migration it is likely 
      that cells are released from cell-cell adhesion only at the lower portion of the 
      cells via modulation of E-cadherin-catenin-based mechanism, and this change 
      allows the cells to extend leading lamellae onto the extracellular matrix 
      substrate remodeled by deposition of fibronectin and organized digestion.
FAU - Nabeshima, K
AU  - Nabeshima K
AD  - Department of Pathology, Miyazaki Medical College, Japan. 
      KAZNABES@post.miyazaki-med.ac.jp
FAU - Inoue, T
AU  - Inoue T
FAU - Shimao, Y
AU  - Shimao Y
FAU - Kataoka, H
AU  - Kataoka H
FAU - Koono, M
AU  - Koono M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Spain
TA  - Histol Histopathol
JT  - Histology and histopathology
JID - 8609357
RN  - 0 (Cadherins)
RN  - EC 3.4.24.- (Metalloendopeptidases)
SB  - IM
MH  - Animals
MH  - Cadherins/metabolism
MH  - Cell Adhesion
MH  - Cell Differentiation
MH  - Cell Movement/physiology
MH  - Colorectal Neoplasms/*pathology
MH  - Extracellular Matrix/metabolism
MH  - Humans
MH  - Metalloendopeptidases/metabolism
MH  - Models, Biological
MH  - Tumor Cells, Cultured
RF  - 118
EDAT- 1999/10/03 00:00
MHDA- 1999/10/03 00:01
CRDT- 1999/10/03 00:00
PHST- 1999/10/03 00:00 [pubmed]
PHST- 1999/10/03 00:01 [medline]
PHST- 1999/10/03 00:00 [entrez]
AID - 10.14670/HH-14.1183 [doi]
PST - ppublish
SO  - Histol Histopathol. 1999 Oct;14(4):1183-97. doi: 10.14670/HH-14.1183.