Leszek Kotula, SUNY Upstate Medical University, USA
Patrycja Dubielecka-Szczerba, Brown University, USA
Cell Communications and Signaling invites you to submit to our new thematic series: Kinases, adaptor proteins, and actin cytoskeleton rearrangements in EMT and cancer.
Epithelial Mesenchymal Transition (EMT) is a complex molecular and cellular process defined by genetic and phenotypic changes in epithelial cells during embryonic development, tissue repair and cancer. EMT is characterized by changes in gene expression and epigenetic programs that profoundly change cellular phenotype and ultimately promote loss of cell-cell adhesion and gain in cell migratory activity. EMT appears to be a strong requisite not only for cancer development but also for metastatic dispersion of primary tumor cells. Comprehensive insight in EMT regulation will not only expand our understanding of tumor development and metastatic processes but it may also inform optimized diagnostics and therapeutic strategies.
Historically, the literature reviewed the role of transcriptional and epigenetic factors that regulate EMT. Here, in this special issue Cell Communication and Signaling, we focus on the molecular and mechanistic links between kinases, adaptor proteins, and actin cytoskeleton as critical components and executors of the EMT regulatory machinery. The EMT transcriptional and epigenetic programs ultimately govern phenotypic changes through actin cytoskeleton rearrangements orchestrated by activation of specific kinases such as SRC or ABL family kinases, or Focal Adhesion Kinase. These signals are then relayed to actin cytoskeleton by adaptor proteins such as ABI1, CRK, EPS8, and other important modulators of cell migration.
Through this review series we hope to shed some more light on mechanistic links between genetic, epigenetic, enzymatic, spatial-signalling regulatory adaptor proteins and actin exoskeleton and their role in execution of phenotypic changes leading to EMT and cancer development and metastasis. We welcome the submission of additional manuscripts to this series.