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CPI-17 drives oncogenic Ras signaling in human melanomas via Ezrin-Radixin-Moesin family proteins

Riecken, LB; Zoch, A; Wiehl, U; Reichert, S; Scholl, I; Cui, Y; Ziemer, M; ... Morrison, H; + view all (2016) CPI-17 drives oncogenic Ras signaling in human melanomas via Ezrin-Radixin-Moesin family proteins. Oncotarget , 7 (48) pp. 78242-78254. 10.18632/oncotarget.12919. Green open access

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Abstract

Hyperactive Ras signaling has strong oncogenic effects causing several different forms of cancer. Hyperactivity is frequently induced by mutations within Ras itself, which account for up to 30% of all human cancers. In addition, hyperactive Ras signaling can also be triggered independent of Ras by either mutation or by misexpression of various upstream regulators and immediate downstream effectors. We have previously reported that C-kinase potentiated protein phosphatase-1 inhibitor of 17 kDa (CPI-17) can drive Ras activity and promote tumorigenic transformation by inhibition of the tumor suppressor Merlin. We now describe an additional element of this oncogenic mechanism in the form of the ezrin-radixin-moesin (ERM) protein family, which exhibits opposing roles in Ras activity control. Thus, CPI-17 drives Ras activity and tumorigenesis in a two-fold way; inactivation of the tumor suppressor merlin and activation of the growth promoting ERM family. The in vivo significance of this oncogenic switch is highlighted by demonstrating CPI-17’s involvement in human melanoma pathogenesis.

Type: Article
Title: CPI-17 drives oncogenic Ras signaling in human melanomas via Ezrin-Radixin-Moesin family proteins
Open access status: An open access version is available from UCL Discovery
DOI: 10.18632/oncotarget.12919
Publisher version: http://dx.doi.org/10.18632/oncotarget.12919
Language: English
Additional information: This work is licensed under a Creative Commons Attribution 3.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material.
Keywords: Science & Technology, Life Sciences & Biomedicine, Oncology, Cell Biology, Cpi-17, Erm, Ras, Cancer, Melanoma, Suppressor Gene-Product, Erm Proteins, Inhibitory Protein, Cell Cortex, Merlin, Growth, Phosphorylation, Phosphatase, Activation, Expression
UCL classification: UCL > Provost and Vice Provost Offices
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences > Div of Biosciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences > Div of Biosciences > Cell and Developmental Biology
URI: https://discovery.ucl.ac.uk/id/eprint/1537383
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