Molecular Analysis of Motility in Metastatic Mammary Adenocarcinoma Cells.
Abstract
To identify sites at which metastasis of breast cancer cells may be interrupted, we are dissecting the process of cell motility in breast cancer cells. Changes in lamellipod extension and chemotaxis in response to EGF were analyzed forMTLn3 cells (a metastatic cell line derived from the 13762NF rat mammary adenocarcinoma). Addition of EGF produced a cessation of ruffling followed by extension of hyaline lamellipods containing increased amounts of F-actin at the growing edge. A nonmetastatic cell line (MTC) derived from the same tumor did not show such responses. Lamellipod extension was maximal within 5 minutes, followed by retraction and resumption of ruffling. Maximal area increases due to lamellipod extension occurred at about 5 nM EGF. Chemotactic and chemokinetic responses were also greatest at 5 nM. Cytochalasin D inhibited EGF-stimulated responses including lamellipod extension, increases in F-actin in lamellipods, and chemotaxis. Nocodazole affected chemotaxis at higher concentrations but not EGF-induced lamellipod extension. We conclude that polymerization of F-actin at the leading edges of lamellipods is necessary for extension of lamellipods and chemotaxis of MTLn3 cells in response to EGF. This work defines the time and concentration ranges of EGF stimulation during which key regulatory proteins are active.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 18, 1995
- Accession Number
- ADA300010
Entities
People
- Jeffrey E. Segall
Organizations
- Albert Einstein College of Medicine