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Abstract
BackgroundPrevious work in our laboratory demonstrated that antiprogestin mifepristone impairs the growth and adhesion of highly metastatic cancer cells, and causes changes in their cellular morphology. In this study, we further assess the anti-metastatic properties of mifepristone, by studying whether cytostatic doses of the drug can inhibit the migration and invasion of various cancer cell lines using a double fluorescence cytochemical labeling approach.MethodsCell lines representing cancers of the ovary (SKOV-3), breast (MDA-MB-231), glia (U87MG), or prostate (LNCaP) were treated with cytostatic concentrations of mifepristone. Wound healing and Boyden chamber assays were utilized to study cellular migration. To study cellular invasion, the Boyden chamber assay was prepared by adding a layer of extracellular matrix over the polycarbonate membrane. We enhanced the assays with the addition of double fluorescence cytochemical staining for fibrillar actin (F-actin) and DNA to observe the patterns of cytoskeletal distribution and nuclear positioning while cells migrate and invade.ResultsWhen exposed to cytostatic concentrations of mifepristone, all cancer cells lines demonstrated a decrease in both migration and invasion capacities measured using standard approaches. Double fluorescence cytochemical labeling validated that mifepristone-treated cancer cells exhibit reduced migration and invasion, and allowed to unveil a distinct migration pattern among the different cell lines, different arrays of nuclear localization during migration, and apparent redistribution of F-actin to the nucleus.ConclusionThis study reports that antiprogestin mifepristone inhibits migration and invasion of highly metastatic cancer cell lines, and that double fluorescence cytochemical labeling increases the value of well-known approaches to study cell movement.
Highlights
Previous work in our laboratory demonstrated that antiprogestin mifepristone impairs the growth and adhesion of highly metastatic cancer cells, and causes changes in their cellular morphology
The changes in cellular morphology and their impact on motility are associated with changes among epithelial and mesenchymal phenotypes, a process known as epithelial-to-mesenchymal transition (EMT)
Mifepristone alters the morphology of cancer cells in a dose-related manner We previously observed, using phase contrast microscopy, that cytostatic concentrations of MF cause elongation of the cytoplasm in various cancer cell types [13]
Summary
Previous work in our laboratory demonstrated that antiprogestin mifepristone impairs the growth and adhesion of highly metastatic cancer cells, and causes changes in their cellular morphology. In turn, is heavily dependent on changes in tumor cell morphology caused by dynamic modifications in the polymerization of actin leading to rearrangements of the cytoskeleton [3]. The transition from an epithelial to a more mesenchymal state is linked to morphological modifications, loss of tight junctions, remodeling of the cytoskeleton, and acquisition of migratory and invasive capacities [4]. Such migratory and invasive capacities are commonly assessed by a variety of experimental approaches which have been amply described [5]
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