Involvement of MINK, a Ste20 family kinase, in Ras oncogene-induced growth arrest in human ovarian surface epithelial cells

Barbara Nicke; Julie Bastien; Sophia J. Khanna; Patricia H. Warne; Victoria Cowling; Simon J. Cook; Gordon Peters; Oona Delpuech; Almut Schulze; Katrien Berns; Jasper Mullenders; Roderick L. Beijersbergen; René Bernards; Trivadi S. Ganesan; Julian Downward; David C. Hancock

doi:10.1016/j.molcel.2005.10.038

Involvement of MINK, a Ste20 family kinase, in Ras oncogene-induced growth arrest in human ovarian surface epithelial cells

Barbara Nicke, Julie Bastien, Sophia J. Khanna, Patricia H. Warne, Victoria Cowling, Simon J. Cook, Gordon Peters, Oona Delpuech, Almut Schulze, Katrien Berns, Jasper Mullenders, Roderick L. Beijersbergen, René Bernards, Trivadi S. Ganesan, Julian Downward, David C. Hancock

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Abstract

The ability of activated Ras to induce growth arrest of human ovarian surface epithelial (HOSE) cells via induction of the cyclin-dependent kinase inhibitor p21^WAF1/CIP1 has been used to screen for Ras pathway signaling components using a library of RNA interference (RNAi) vectors targeting the kinome. Two known Ras-regulated kinases were identified, phosphoinositide 3-kinase p110a and ribosomal protein S6 kinase p70^S6K1, plus the MAP kinase kinase kinase kinase MINK, which had not previously been implicated in Ras signaling. MINK is activated after Ras induction via a mechanism involving reactive oxygen species and mediates stimulation of the stress-activated protein kinase p38 MAPK downstream of the Raf/ERK pathway. p38 MAPK activation is essential for Ras-induced p21^WAF1/CIP1 upregulation and cell cycle arrest. MINK is thus a distal target of Ras signaling in the induction of a growth-arrested, senescent-like phenotype that may act to oppose oncogenic transformation in HOSE cells.

Original language	English
Pages (from-to)	673-85
Number of pages	13
Journal	Molecular Cell
Volume	20
Issue number	5
DOIs	https://doi.org/10.1016/j.molcel.2005.10.038
Publication status	Published - 2005

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Nicke, B., Bastien, J., Khanna, S. J., Warne, P. H., Cowling, V., Cook, S. J., Peters, G., Delpuech, O., Schulze, A., Berns, K., Mullenders, J., Beijersbergen, R. L., Bernards, R., Ganesan, T. S., Downward, J., & Hancock, D. C. (2005). Involvement of MINK, a Ste20 family kinase, in Ras oncogene-induced growth arrest in human ovarian surface epithelial cells. Molecular Cell, 20(5), 673-85. https://doi.org/10.1016/j.molcel.2005.10.038

@article{d7bcf0cbf6cf4e7390c4df5e7288b44d,

title = "Involvement of MINK, a Ste20 family kinase, in Ras oncogene-induced growth arrest in human ovarian surface epithelial cells",

abstract = "The ability of activated Ras to induce growth arrest of human ovarian surface epithelial (HOSE) cells via induction of the cyclin-dependent kinase inhibitor p21WAF1/CIP1 has been used to screen for Ras pathway signaling components using a library of RNA interference (RNAi) vectors targeting the kinome. Two known Ras-regulated kinases were identified, phosphoinositide 3-kinase p110a and ribosomal protein S6 kinase p70S6K1, plus the MAP kinase kinase kinase kinase MINK, which had not previously been implicated in Ras signaling. MINK is activated after Ras induction via a mechanism involving reactive oxygen species and mediates stimulation of the stress-activated protein kinase p38 MAPK downstream of the Raf/ERK pathway. p38 MAPK activation is essential for Ras-induced p21WAF1/CIP1 upregulation and cell cycle arrest. MINK is thus a distal target of Ras signaling in the induction of a growth-arrested, senescent-like phenotype that may act to oppose oncogenic transformation in HOSE cells.",

author = "Barbara Nicke and Julie Bastien and Khanna, {Sophia J.} and Warne, {Patricia H.} and Victoria Cowling and Cook, {Simon J.} and Gordon Peters and Oona Delpuech and Almut Schulze and Katrien Berns and Jasper Mullenders and Beijersbergen, {Roderick L.} and Ren{\'e} Bernards and Ganesan, {Trivadi S.} and Julian Downward and Hancock, {David C.}",

year = "2005",

doi = "10.1016/j.molcel.2005.10.038",

language = "English",

volume = "20",

pages = "673--85",

journal = "Molecular Cell",

issn = "1097-2765",

publisher = "Cell Press",

number = "5",

}

Nicke, B, Bastien, J, Khanna, SJ, Warne, PH, Cowling, V, Cook, SJ, Peters, G, Delpuech, O, Schulze, A, Berns, K, Mullenders, J, Beijersbergen, RL, Bernards, R, Ganesan, TS, Downward, J & Hancock, DC 2005, 'Involvement of MINK, a Ste20 family kinase, in Ras oncogene-induced growth arrest in human ovarian surface epithelial cells', Molecular Cell, vol. 20, no. 5, pp. 673-85. https://doi.org/10.1016/j.molcel.2005.10.038

TY - JOUR

T1 - Involvement of MINK, a Ste20 family kinase, in Ras oncogene-induced growth arrest in human ovarian surface epithelial cells

AU - Nicke, Barbara

AU - Bastien, Julie

AU - Khanna, Sophia J.

AU - Warne, Patricia H.

AU - Cowling, Victoria

AU - Cook, Simon J.

AU - Peters, Gordon

AU - Delpuech, Oona

AU - Schulze, Almut

AU - Berns, Katrien

AU - Mullenders, Jasper

AU - Beijersbergen, Roderick L.

AU - Bernards, René

AU - Ganesan, Trivadi S.

AU - Downward, Julian

AU - Hancock, David C.

PY - 2005

Y1 - 2005

N2 - The ability of activated Ras to induce growth arrest of human ovarian surface epithelial (HOSE) cells via induction of the cyclin-dependent kinase inhibitor p21WAF1/CIP1 has been used to screen for Ras pathway signaling components using a library of RNA interference (RNAi) vectors targeting the kinome. Two known Ras-regulated kinases were identified, phosphoinositide 3-kinase p110a and ribosomal protein S6 kinase p70S6K1, plus the MAP kinase kinase kinase kinase MINK, which had not previously been implicated in Ras signaling. MINK is activated after Ras induction via a mechanism involving reactive oxygen species and mediates stimulation of the stress-activated protein kinase p38 MAPK downstream of the Raf/ERK pathway. p38 MAPK activation is essential for Ras-induced p21WAF1/CIP1 upregulation and cell cycle arrest. MINK is thus a distal target of Ras signaling in the induction of a growth-arrested, senescent-like phenotype that may act to oppose oncogenic transformation in HOSE cells.

AB - The ability of activated Ras to induce growth arrest of human ovarian surface epithelial (HOSE) cells via induction of the cyclin-dependent kinase inhibitor p21WAF1/CIP1 has been used to screen for Ras pathway signaling components using a library of RNA interference (RNAi) vectors targeting the kinome. Two known Ras-regulated kinases were identified, phosphoinositide 3-kinase p110a and ribosomal protein S6 kinase p70S6K1, plus the MAP kinase kinase kinase kinase MINK, which had not previously been implicated in Ras signaling. MINK is activated after Ras induction via a mechanism involving reactive oxygen species and mediates stimulation of the stress-activated protein kinase p38 MAPK downstream of the Raf/ERK pathway. p38 MAPK activation is essential for Ras-induced p21WAF1/CIP1 upregulation and cell cycle arrest. MINK is thus a distal target of Ras signaling in the induction of a growth-arrested, senescent-like phenotype that may act to oppose oncogenic transformation in HOSE cells.

U2 - 10.1016/j.molcel.2005.10.038

DO - 10.1016/j.molcel.2005.10.038

M3 - Article

C2 - 16337592

SN - 1097-2765

VL - 20

SP - 673

EP - 685

JO - Molecular Cell

JF - Molecular Cell

IS - 5

ER -

Involvement of MINK, a Ste20 family kinase, in Ras oncogene-induced growth arrest in human ovarian surface epithelial cells

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