Rho GTPases and cancer

Li, Hui; Peyrollier, Karine; Kilic, Gülcan; Brakebusch, Cord

doi:10.1002/biof.1155

Cited by 55 publications

(50 citation statements)

References 100 publications

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“…Furthermore, DNM2 regulates Golgi structure and vesiculation during the secretory process which can affect trafficking of other carcinogenic signaling molecules36. Finally, DNM2 interacts with F-actin and actin dynamics, actin-associated proteins, and molecules that induce or sense membrane curvature as well as expression of angiogenic receptors3738. Our study shows high DNM2 -expression in persons with ALL.…”

Section: Discussionmentioning

confidence: 66%

Targeting High Dynamin-2 (DNM2) Expression by Restoring Ikaros Function in Acute Lymphoblastic Leukemia

Han

et al. 2016

Sci Rep

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Dynamin-2 (DNM2) is a GTPase essential for intracellular vesicle formation and trafficking, cytokinesis and receptor endocytosis. Mutations in DNM2 are common in early T-cell precursor acute lymphoblastic leukemia. However, DNM2 expression in other types of ALL are not reported. We studied DNM2 mRNA level in adults with B- and T-cell ALL. We found DNM2 is more highly expressed compared with normals in both forms of ALL. High DNM2 expression is associated with some clinical and laboratory features, inferior outcomes and with leukaemia cell proliferation. We also found Ikaros directly binds the DNM2 promoter and suppresses DNM2 expression. Consequently IKZF1 deletion is associated with high DNM2 expression. Conversely, casein kinase-2 (CK2)-inhibitor increases Ikaros function thereby inhibiting DNM2 expression. Inhibiting DNM2 suppresses proliferation of leukemia cells and synergizes with CK2 inhibition. Our data indicate high DNM2 expression is associated with Ikaros dysregulation and may be important in the development of B-ALL.

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Section: Discussionmentioning

confidence: 66%

Targeting High Dynamin-2 (DNM2) Expression by Restoring Ikaros Function in Acute Lymphoblastic Leukemia

Han

et al. 2016

Sci Rep

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“…Rho proteins and ROCK proteins are important regulators of cell migration, proliferation and apoptosis [24]. Activated ROCK1 by Rho GTPase family member binds and phosphorylates AKT, PTEN, FAK [25, 26].…”

Section: Discussionmentioning

confidence: 99%

YMO1 suppresses invasion and metastasis by inhibiting RhoC signaling and predicts favorable prognosis in hepatocellular carcinoma

et al. 2016

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Previous studies have shown that 4.1 proteins, which are deregulated in many cancers, contribute to cell adhesion and motility. Yurt/Mosaic eyes-like 1 (YMO1) is a member of 4.1 protein family but it is unclear whether YMO1 plays a role in tumor invasion. This study aimed to investigate the effects of YMO1 on hepatocellular carcinoma (HCC) and attempted to elucidate the underlying molecular mechanisms. YMO1 expression in HCC tissues and its correlation with clinicopathological features and postoperative prognosis was analyzed. The results showed that YMO1 was down-regulated in the highly metastatic HCC cell line and in human tumor tissues. Underexpression of YMO1 indicated poor prognosis of HCC patients. Restoration of YMO1 expression caused a significant decrease in cell migration and invasiveness in vitro. In vivo study showed that YMO1 reduced liver tumor invasion and metastasis in xenograft mice. YMO1 directly inhibited RhoC activation. YMO1 expression in HCC was regulated by PAX5. Analysis of YMO1 expression levels in human HCC patients revealed a significant correlation of YMO1 expression with PAX5 and RhoC. Our findings revealed that YMO1 predicts favorable prognosis and the data suggest that YMO1 suppresses tumor invasion and metastasis by inhibiting RhoC activity.

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“…6, 7 Evidence that they are pro-neoplastic emerged over 20 years ago with studies showing that constitutively active RhoA and Rac1 mutants possess weak transforming activity. 8–10 Dominant negative forms of Rho GTPases could block K-Ras or other oncogene-driven transformation of fibroblasts, suggesting an interconnection between Rho and Ras signaling pathways.…”

Section: Introductionmentioning

confidence: 99%

Rho GTPases: Anti- or pro-neoplastic targets?

et al. 2016

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Rho GTPases are critical signal transducers of multiple pathways. They have been proposed to be useful anti-neoplastic targets for over two decades, especially in Ras-driven cancers. Until recently, however, few in vivo studies had been carried out to test this premise. Several recent mouse model studies have verified that Rac1, RhoA, and some of their effector proteins such as PAK and ROCK, are likely anti-cancer targets for treating K-Ras-driven tumors. Other seemingly contradictory studies have suggested that at least in certain instances inhibition of individual Rho GTPases may paradoxically result in pro-neoplastic effects. Significantly, both RhoA GTPase gain- and loss-of-function mutations have been discovered in primary leukemia/lymphoma and gastric cancer by human cancer genome sequencing efforts, suggesting both pro- and anti-neoplastic roles. In this review we summarize and integrate these unexpected findings and discuss the mechanistic implications in the design and application of Rho GTPase targeting strategies in future cancer therapies.

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Rho GTPases and cancer

Cited by 55 publications

References 100 publications

Targeting High Dynamin-2 (DNM2) Expression by Restoring Ikaros Function in Acute Lymphoblastic Leukemia

Targeting High Dynamin-2 (DNM2) Expression by Restoring Ikaros Function in Acute Lymphoblastic Leukemia

YMO1 suppresses invasion and metastasis by inhibiting RhoC signaling and predicts favorable prognosis in hepatocellular carcinoma

Rho GTPases: Anti- or pro-neoplastic targets?

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