p120-catenin differentially regulates cell migration by Rho-dependent intracellular and secreted signals

Research output: Contribution to journalJournal articleResearchpeer-review

The adherens junction protein p120-catenin is implicated in the regulation of cadherin stability, cell migration and inflammatory responses in mammalian epithelial tissues. How these events are coordinated to promote wound repair is not understood. We show that p120 catenin regulates the intrinsic migratory properties of primary mouse keratinocytes, but also influences the migratory behavior of neighboring cells by secreted signals. These events are rooted in the ability of p120-catenin to regulate RhoA GTPase activity, which leads to a two-tiered control of cell migration. One restrains cell motility via an increase in actin stress fibers, reduction in integrin turnover and an increase in the robustness of focal adhesions. The other is coupled to the secretion of inflammatory cytokines including interleukin-24, which causally enhances randomized cell movements. Taken together, our results indicate that p120-RhoA-GTPase-mediated signaling can differentially regulate the migratory behavior of epidermal cells, which has potential implications for chronic wound responses and cancer.

Original languageEnglish
JournalE M B O Reports
Volume15
Issue number5
Pages (from-to)592-600
Number of pages9
ISSN1469-221X
DOIs
Publication statusPublished - 2014
Externally publishedYes

    Research areas

  • Actin Cytoskeleton, Animals, Catenins, Cell Adhesion, Cell Movement, Cells, Cultured, Focal Adhesions, Integrins, Interleukins, Keratinocytes, Mice, Signal Transduction, Wound Healing, rho GTP-Binding Proteins, Journal Article, Research Support, Non-U.S. Gov't

ID: 188368503