Abstract
Despite great improvements in the diagnosis and treatment of neoplasms, metastatic disease is still the leading cause of death in cancer patients, with mortality rates still rising. Given this background, new ways to treat cancer will be important for development of improved cancer control strategies. Cdc42 is a member of the Rho GTPase family and plays an important role in cell-to-cell adhesion, formation of cytoskeletal structures, and cell cycle regulation. It thus influences cellular proliferation, transformation, and homeostasis, as well as the cellular migration and invasion processes underlying tumor formation. Cdc42 acts as a collection point for signal transduction and regulates multiple signaling pathways. Moreover, recent studies show that in most human cancers Cdc42 is abnormally expressed and promoting neoplastic growth and metastasis. Regarding possible new treatments for cancer, miRNA and small molecules targeting Cdc42 and related pathways have been recently found to be effective on cancer. In this review, we analyze the newly recognized regulation mechanisms for Cdc42 and Cdc42-related signal pathways, and particularly new treatments using small molecules and miRNAs to inhibit the abnormal overexpression of Cdc42 that may slow down the metastasis process, improve cancer therapy and lead to novel strategies for development of antineoplastic drugs.
Highlights
Cell division control protein 42 homolog (Cdc42) is a member of the Rho GTPase family, which was first discovered in Saccharomyces cerevisiae cells, where it was found to be a marker of the loci where new buds would appear
Zhang et al [110] found that overexpression of miR-224 could promote viability and migration in hepatocellular carcinoma (HCC) cells, which decreased the expression of Cdc42, CDH1, and PAK2 and increased the expression of BCL-2
It is clear that Cdc42 and its signaling pathways play important roles in tumor invasion, metastasis, and proliferation
Summary
Cell division control protein 42 homolog (Cdc42) is a member of the Rho GTPase family, which was first discovered in Saccharomyces cerevisiae cells, where it was found to be a marker of the loci where new buds would appear. GAPs play a negative regulatory role on the activity of Cdc via hydrolysis of GTP to GDP; GDIs lock the GDP-bound inactive state of Cdc and prevent its further activation [3]. This is the classic “GTPase cycle” model of Cdc (Figure 1). Based on this mechanism, many small molecule inhibitors have been developed that are targeted to Cdc and its signaling proteins [4]. GEFs, GAPs, and GDIs. When Cdc is activated by various stimuli, Cdc can transiently interact with its downstream effector proteins, triggering cytoskeleton reorganization, alterations in the cell cycle, and transcription
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