Abstract
Cofilin is an actin-binding protein that regulates filament dynamics and depolymerization. The over-expression of cofilin is observed in various cancers, cofilin promotes cancer metastasis by regulating cytoskeletal reorganization, lamellipodium formation and epithelial-to-mesenchymal transition. Clinical treatment of cancer regarding cofilin has been explored in aspects of tumor cells apoptosis and cofilin related miRNAs. This review addresses the structure and phosphorylation of cofilin and describes recent findings regarding the function of cofilin in regulating cancer metastasis and apoptosis in tumor cells.
Highlights
Actin-binding proteins are abundant cellular proteins that regulate cell function by mediating actin polymerization and remodeling (Dos Remedios et al, 2003; Virtanen and Vartiainen, 2017)
Cofilin is known as a regulator of actin filament dynamics, it is a small protein of ∼21 kDA that is ubiquitously expressed in all vertebrates and freely diffuses in eukaryotic cells (Shishkin et al, 2016)
Cofilin was found to be the major protein in different human cancer cells that can modulate cellular morphology, mitosis and mitochondrial fission
Summary
Actin-binding proteins are abundant cellular proteins that regulate cell function by mediating actin polymerization and remodeling (Dos Remedios et al, 2003; Virtanen and Vartiainen, 2017). Cofilin is an actin-binding protein and is function as a severing protein that severs actin filaments (Wang et al, 2007; Huang et al, 2014; Chang et al, 2015). Cofilin is known as a regulator of actin filament dynamics, it is a small protein of ∼21 kDA that is ubiquitously expressed in all vertebrates and freely diffuses in eukaryotic cells (Shishkin et al, 2016). Once cofilin is activated by dephosphorylation, it servers actin by translocating into the nucleus with binding to actin (Ishikawa-Ankerhold et al, 2017). Cofilin promotes the cell motility by regulating the cytoskeletal reorganization, promoting the lamellipodium formation, cell–cell adhesion dissolution, epithelial-to-mesenchymal transition (EMT) process and “migration-by-tethering” mechanism, participate in the cancer metastasis. This review discusses the functional role of cofilin in cancer metastasis and provides evidence for clinical perspective of cofilin in cancer treatment
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