PortalPublikationenCPI-17 drives oncogenic Ras signaling in human melanomas via...

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

Standard

CPI-17 drives oncogenic Ras signaling in human melanomas via Ezrin-Radixin-Moesin family proteins. / Lars Björn, Riecken; Zoch, Ansgar; Wiehl, Ulrike; Reichert, Sabine; Scholl, Ingmar; Cui, Yan; Ziemer, Mirjana; Anderegg, Ulf; Hagel, Christian; Morrison, Helen.

in: ONCOTARGET, Jahrgang 7, Nr. 48, 29.11.2016, S. 78242-78254.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Lars Björn, R, Zoch, A, Wiehl, U, Reichert, S, Scholl, I, Cui, Y, Ziemer, M, Anderegg, U, Hagel, C & Morrison, H 2016, 'CPI-17 drives oncogenic Ras signaling in human melanomas via Ezrin-Radixin-Moesin family proteins', ONCOTARGET, Jg. 7, Nr. 48, S. 78242-78254. https://doi.org/10.18632/oncotarget.12919

APA

Lars Björn, R., Zoch, A., Wiehl, U., Reichert, S., Scholl, I., Cui, Y., Ziemer, M., Anderegg, U., Hagel, C., & Morrison, H. (2016). CPI-17 drives oncogenic Ras signaling in human melanomas via Ezrin-Radixin-Moesin family proteins. ONCOTARGET, 7(48), 78242-78254. https://doi.org/10.18632/oncotarget.12919

Vancouver

Lars Björn R, Zoch A, Wiehl U, Reichert S, Scholl I, Cui Y et al. CPI-17 drives oncogenic Ras signaling in human melanomas via Ezrin-Radixin-Moesin family proteins. ONCOTARGET. 2016 Nov 29;7(48):78242-78254. https://doi.org/10.18632/oncotarget.12919

Bibtex

@article{ef0b8cc78cc54af0904f9737ac0ddbbd,
title = "CPI-17 drives oncogenic Ras signaling in human melanomas via Ezrin-Radixin-Moesin family proteins",
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.",
author = "{Lars Bj{\"o}rn}, Riecken and Ansgar Zoch and Ulrike Wiehl and Sabine Reichert and Ingmar Scholl and Yan Cui and Mirjana Ziemer and Ulf Anderegg and Christian Hagel and Helen Morrison",
year = "2016",
month = nov,
day = "29",
doi = "10.18632/oncotarget.12919",
language = "English",
volume = "7",
pages = "78242--78254",
journal = "ONCOTARGET",
issn = "1949-2553",
publisher = "IMPACT JOURNALS LLC",
number = "48",

}

RIS

TY - JOUR

T1 - CPI-17 drives oncogenic Ras signaling in human melanomas via Ezrin-Radixin-Moesin family proteins

AU - Lars Björn, Riecken

AU - Zoch, Ansgar

AU - Wiehl, Ulrike

AU - Reichert, Sabine

AU - Scholl, Ingmar

AU - Cui, Yan

AU - Ziemer, Mirjana

AU - Anderegg, Ulf

AU - Hagel, Christian

AU - Morrison, Helen

PY - 2016/11/29

Y1 - 2016/11/29

N2 - 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.

AB - 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.

U2 - 10.18632/oncotarget.12919

DO - 10.18632/oncotarget.12919

M3 - SCORING: Journal article

C2 - 27793041

VL - 7

SP - 78242

EP - 78254

JO - ONCOTARGET

JF - ONCOTARGET

SN - 1949-2553

IS - 48

ER -