Abstract
Myosin is a kind of actin-based motor protein. As the crucial functions of myosin during tumorigenesis have become increasingly apparent, the profile of myosin in the field of cancer research has also been growing. Eighteen distinct classes of myosins have been discovered in the past twenty years and constitute a diverse superfamily. Various myosins share similar structures. They all convert energy from ATP hydrolysis to exert mechanical stress upon interactions with microfilaments. Ongoing research is increasingly suggesting that at least seven kinds of myosins participate in the formation and development of cancer. Myosins play essential roles in cytokinesis failure, chromosomal and centrosomal amplification, multipolar spindle formation and DNA microsatellite instability. These are all prerequisites of tumor formation. Subsequently, myosins activate various processes of tumor invasion and metastasis development including cell migration, adhesion, protrusion formation, loss of cell polarity and suppression of apoptosis. In this review, we summarize the current understanding of the roles of myosins during tumorigenesis and discuss the factors and mechanisms which may regulate myosins in tumor progression. Furthermore, we put forward a completely new concept of “chromomyosin” to demonstrate the pivotal functions of myosins during karyokinesis and how this acts to optimize the functions of the members of the myosin superfamily.
Highlights
Carcinogenesis is a multifaceted and complex process involving alterations in genetic or chromosomal stability [1] that disrupt the normal processes of cell growth and apoptosis progression [2] and propel the formation of malignant tumors [3]
We summarize nine distinctive pathways and myosins related up- or down-stream molecules, including myosin light chain kinase (MLCK), Pyruvate kinase M2 (PKM2), Sds22, Cdc42, integrin-β1, syndecan-4, merlin, RhoGTP exchange factor (RhoGEF2), Rho GTPases and phytate hydrolysate, etc
Ample evidence supports the roles of myosins in cell adhesion and cancer invasion, detailed studies are still required to elucidate the related specific molecular mechanisms and to elucidate the other interacting proteins involved in myosin-related cancer cell migration and metastasis development
Summary
Carcinogenesis is a multifaceted and complex process involving alterations in genetic or chromosomal stability [1] that disrupt the normal processes of cell growth and apoptosis progression [2] and propel the formation of malignant tumors [3]. The impairing of p53 can promote increased myosin X expression levels, myosin X being responsible for cell adhesion inhibition, protrusion formation and tumor progression [55]. In addition to tumor cells, centrosome amplification and associated multipolar mitoses takes place in the early stages of inflammation [69] These studies indicate that the CIN and cytokinesis failures, together with the related chromosomal and centrosomal amplifications, play crucial roles in tumorigenesis and cancer development. There are some experimental results indicating that myosins are required for various other cellular functions related to the formation of cancer These include cell migration and tumor metastasis. Ample evidence supports the roles of myosins in cell adhesion and cancer invasion, detailed studies are still required to elucidate the related specific molecular mechanisms and to elucidate the other interacting proteins involved in myosin-related cancer cell migration and metastasis development. This suggests that the integrin-myosin X interaction is an irreplaceable factor during protrusion formation and cell motility (See Figure 4)
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