Class I Myosins, molecular motors involved in cell migration and cancer

Figures

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  Figure 1.. Class I myosin family structural organization and tissue expression. a) Schematic representation of the class I myosin family highlighting the main structural domains, Motor, Neck and Tail. b) Class I myosin gene expression heatmaps constructed with GTEX v8 (24 tissues), note the highly restricted expression pattern of Myo1h, Myo1a and Myo1g and the widely distributed expression of the remaining five class I myosins.

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  Figure 2.. Leukemic cells produce extramedullary infiltrates in Central Nervous System and Testis. Patients with Acute Lymphoblastic Leukemia that present infiltrations at diagnosis are classified as high-risk patients. The severity of the patient’s condition is related to the presence of infiltrates, neutropenia, thrombocytopenia, hemorrhages, and acute anemia; Thrombocytopenia results in a decrease in blood volume due to frequent bleedings in patients. The decrease in blood volume creates a pathophysiological environment conducive to the formation of infiltrates and this combined with intrinsically improved cell migration characteristics of the leukemic cells due to over expression of Myo1g that increases plasma membrane tension and upregulation of adhesion molecules such as CD44 (dotted square) will result in infiltration into the CNS and testis in high-risk patients.

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  Figure 3.. Class I myosin expression in 20 different cancer types, data from Oncomine, note differential expression of the class I Myosins, in lanes 5 and 20 corresponding to Acute Lymphoblastic Leukemia from B (5) and T (20) Cell origin, compared with the rest of different cancer types. Myo1h is not present in the database.