Protein Kinase C, Focal Adhesions and the Regulation of Cell Migration

Abstract

Cell adhesion to extracellular matrix is a complex process involving protrusive activity driven by the actin cytoskeleton, engagement of specific receptors, followed by signaling and cytoskeletal organization. Thereafter, contractile and endocytic/recycling activities may facilitate migration and adhesion turnover. Focal adhesions, or focal contacts, are widespread organelles at the cell-matrix interface. They arise as a result of receptor interactions with matrix ligands, together with clustering. Recent analysis shows that focal adhesions contain a very large number of protein components in their intracellular compartment. Among these are tyrosine kinases, which have received a great deal of attention, whereas the serine/threonine kinase protein kinase C has received much less. Here the status of protein kinase C in focal adhesions and cell migration is reviewed, together with discussion of its roles and potential substrates.

Inhibition of invasion by glycogen synthase kinase-3 beta inhibitors through dysregulation of actin re-organisation via down-regulation of WAVE2

“…Cellular attachment to surfaces of culture vessels is maintained by cell-extracellular matrix attachment machinery called focal adhesion [22]; therefore, we examined focal adhesion after GSK-3b inhibition. Immunocytostaining against vinculin revealed that focal adhesion tended to become larger after AR-A0114418 treatment in MDA-MB-231 cells ( Fig.…”

“…Focal adhesion tethers the intracellular actin cytoskeleton to the extracellular matrix [22]. We investigated changes in the actin cytoskeleton after treatment with GSK-3b inhibitors.…”

Antitumor Studies of Earthworm Fibrinolytic Enzyme Component A from Eisenia foetida on Breast Cancer Cell Line MCF-7

“…The invasion, progression and metastasis of tumor cells was closely related to cell adhesion between the extracellular matrix and other cells [30] . Cell adhesion was dependent on cell adhesion molecules and kinase [31,32] . FAK, a non-receptor binding to tyrosine kinase, which could regulate focal adhesion formation and disassembly, is involved in tumour initiation and progression, including cell survival and apoptosis, adhesion, migration and invasion [33][34][35][36] .…”

Functional interaction of PkcA and PldB regulate aggregation and development in Dictyostelium discoideum

“…In addition to regulating cytoskeletal organization, Protein Kinase C isoforms are regulators of nuclear segregation[21,39,40]. To determine whether pkcA plays a role during nuclear segregation, we looked at the multinuclearity state of populations of vegetative cells (Fig.…”