Regulation of glioblastoma cell invasion by PKC iota and RhoB

Oncogene
R M BaldwinI A J Lorimer

Abstract

Glioblastoma multiforme is the most aggressive form of primary brain tumor and remains largely incurable, in large part, due to its highly invasive nature. The phosphoinositide (PI) 3-kinase pathway is often constitutively active in these tumors due to activating mutations in the epidermal growth factor receptor, or deletion/loss of function of the tumor suppressor PTEN. Protein kinase C type iota (PKC iota), a member of the atypical protein kinase C family, is activated by the PI 3-kinase pathway and is an important downstream mediator. Here, we have assessed the role of PKC iota in glioblastoma cell invasion. Depletion of PKC iota with RNA interference caused an increase in actin stress fibers and a decrease in cell motility and invasion. Gene expression microarray analysis of U87MG cells showed that PKC iota repressed expression of mRNA for RhoB, which has previously been shown to have a role in actin stress fiber formation. Western blot analysis showed that both PKC iota depletion and pharmacological inhibition of PKC iota caused an increase in the protein levels of RhoB, as did inhibition of PI 3-kinase. Expression of RhoB from a constitutive promoter caused changes in actin stress fibers and cell invasion that were simila...Continue Reading

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Citations

Nov 29, 2011·Oncogene·J A PagetI A J Lorimer
Sep 9, 2010·Cell Communication and Signaling : CCS·Matteo Parri, Paola Chiarugi
Oct 7, 2009·Proceedings of the National Academy of Sciences of the United States of America·Hitoshi IshiguroHiroji Uemura
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May 1, 2021·Biomedicines·Noelia Geribaldi-DoldánCarmen Castro

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