| Melanoma is an aggressive cancer with increasing incidence and a growing lifetime risk that arises from normal melanocytes or their precursors.Melanoma has the characteristics of unlimited replication,increased melanin content,rapid proliferation and resistance to apoptosis.A thorough understanding of the molecular mechanism of melanomagenesis and melanoma biology is essential for the diagnosis,prognostication,and therapy of melanoma.Cyclin-dependent protein kinase 5(Cdk5)is one of the proteins highly expressed in B16-F10 melanoma cells that controls melanoma cell motility,invasiveness,and metastatic spread,and might be a promising novel therapeutic target.Cdk5 is guided by proline serine/threonine kinase,despite its c DNA was first cloned dependencies for the cell cycle protein kinase(Cdk)the homologous genes of the other members of the family,but the function of Cdk5 has proved to be different from other Cdks Cdk5 was not partners in the cell cycle protein p35 and p39 activation,through affecting the adhesive migration and differentiation of neurons play an important role in the process of brain development.The effect of Cdk5 on proliferation and migration,which are important for carcinogenesis,has not been reported.In the current study,we found that si RNA-mediated knockdown of Cdk5 in B16-F10 melanoma cells inhibited melanoma cell proliferation through downregulation of the Ca MK4-p-CREB pathway,inhibited migration through downregulation of p-CREB,integrin beta 1,and integrin beta 5,and also inhibited tyrosinase activity and melanins production through p-CREB-MITF regulation.The results indicate that Cdk5 controls melanoma development,with an essential regulatory role for p-CREB. |
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