Abstract
BackgroundThe collective cell migration of stratified epithelial cells is considered to be an important phenomenon in wound healing, development, and cancer invasion; however, little is known about the mechanisms involved. Furthermore, whereas Rho family proteins, including RhoA, play important roles in cell migration, the exact role of Rho-associated coiled coil-containing protein kinases (ROCKs) in cell migration is controversial and might be cell-type dependent. Here, we report the development of a novel modified scratch assay that was used to observe the collective cell migration of stratified TE-10 cells derived from a human esophageal cancer specimen.ResultsDesmosomes were found between the TE-10 cells and microvilli of the surface of the cell sheet. The leading edge of cells in the cell sheet formed a simple layer and moved forward regularly; these rows were followed by the stratified epithelium. ROCK inhibitors and ROCK small interfering RNAs (siRNAs) disturbed not only the collective migration of the leading edge of this cell sheet, but also the stratified layer in the rear. In contrast, RhoA siRNA treatment resulted in more rapid migration of the leading rows and disturbed movement of the stratified portion.ConclusionsThe data presented in this study suggest that ROCKs play an important role in mediating the collective migration of TE-10 cell sheets. In addition, differences between the effects of siRNAs targeting either RhoA or ROCKs suggested that distinct mechanisms regulate the collective cell migration in the simple epithelium of the wound edge versus the stratified layer of the epithelium.Electronic supplementary materialThe online version of this article (doi:10.1186/s40659-015-0039-2) contains supplementary material, which is available to authorized users.
Highlights
The collective cell migration of stratified epithelial cells is considered to be an important phenomenon in wound healing, development, and cancer invasion; little is known about the mechanisms involved
We describe a novel method to observe the collective migration of stratified cells on glass coverslips. Using this method to investigate the effects of Rho family proteins on collective cell migration, we found that the inhibition of Rho-associated coiled coil-containing protein kinases (ROCK) suppressed the collective migration of TE-10 cells, a cell line derived from human esophageal cancer tissue
We concluded that TE-10 cells were able to form a stratified epithelial sheet under the growth conditions used
Summary
The collective cell migration of stratified epithelial cells is considered to be an important phenomenon in wound healing, development, and cancer invasion; little is known about the mechanisms involved. Whereas Rho family proteins, including RhoA, play important roles in cell migration, the exact role of Rho-associated coiled coil-containing protein kinases (ROCKs) in cell migration is controversial and might be cell-type dependent. The collective migration of epithelial cells is an important phenomenon in wound healing [1, 2], development [3,4,5], and cancer invasion [6,7,8]. In a study using clinical samples collected from patients with esophageal cancer, ROCK inhibition suppressed the invasion and metastasis of esophageal cancer cells [31], suggesting the importance of ROCKs in esophageal cancer progression
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