The diverse roles of Rac signaling in tumorigenesis

Mack, Natalie A.; Whalley, Helen J.; Castillo-Lluva, Sonia; Malliri, Angeliki

doi:10.4161/cc.10.10.15612

Cited by 138 publications

(142 citation statements)

References 121 publications

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“…Activation of Rac1 GTPase can induce EMT, and regulate the expression of MMPs (Mack et al, 2011). It is reported that TIAM2 is required for the activation of Rac1 GTPase in neuronal and skin papilloma cells (Matsuo et al, 2002;Rooney et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

TIAM2 Enhances Non-small Cell Lung Cancer Cell Invasion and Motility

Zhao

Han²,

Liu³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Background: TIAM2, a Rac guanine nucleotide exchange factor, is closely associated with cell adherence and migration. Here, we aimed to investigate the role of TIAM2 in non-small cell lung cancer (NSCLC) cells. Materials and Methods: A small interference RNA (siRNA) was introduced to silence the expression of TIAM2. Invasion and motility assays were then performed to assess the invasion and motility potential of NSCLC cells. GST-pull down assays were used to detect activation of Rac1. Results: TIAM2 was highly expressed in NSCLC cells. Knockdown of TIAM2 inhibited the invasion and motility, and suppressed activation of Rac1. Further experiments demonstrated that knockdown of TIAM2 could up-regulate the expression of E-cadherin, and downregulate the expression of MMP-3, Twist and Snail. Conclusions: Our data suggest that TIAM2 can promote invasion and motility of NSCLC cells. Activation of Rac1 and regulation of some EMT/invasion-related genes may be involved in the underlying processes.

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Section: Discussionmentioning

confidence: 99%

TIAM2 Enhances Non-small Cell Lung Cancer Cell Invasion and Motility

Zhao

Han²,

Liu³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…We anticipate that this concept may allow targeting of other small GTPases as well. For example, with respect to cancer, it might be useful to develop inhibitors against Rac and Rho family members, because Rac and Rho are often overexpressed in cancer cells to support altered tumor physiology (42)(43)(44). Indeed, it has been shown that misregulation of Rac and Rho signaling leads to disruption of junctions and actin cytoskeleton reorganization, allowing cancer cell migration and invasion (45).…”

Section: Discussionmentioning

confidence: 99%

In situ selectivity profiling and crystal structure of SML-8-73-1, an active site inhibitor of oncogenic K-Ras G12C

Hunter¹,

Gurbani²,

Ficarro

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

205

183

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Significance SML-8-73-1 (SML) is the first example, to our knowledge, of a GTP-competitive inhibitor of V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (K-Ras). A high-resolution structure of K-Ras G12C bound to SML shows K-Ras in an inactive conformation. In situ proteomic-based chemical profiling of SML demonstrates that SML is highly selective for K-Ras G12C over other small GTPases. A novel chemosensor-based assay allows measurement of covalent reaction rates between K-Ras G12C and SML and enables characterization of this reaction in the context of millimolar concentrations of GTP and GDP, well in exccss of what is found in living cells. These results demonstrate that even in the presence of high concentrations of GTP and GDP, SML is able to exchange into the GN site.

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“…tion, and migration (15,49), the findings from current and previous studies suggest that deregulation of Rac1 expression and activity may play important roles in arsenic carcinogenesis.…”

Section: Discussionmentioning

confidence: 75%