RSK is a principal effector of the RAS-ERK pathway for eliciting a coordinate promotile/invasive gene program and phenotype in epithelial cells

Ulrik Doehn, Camilla Hauge, Scott R Frank, Claus J Jensen, Katarzyna Duda, Jakob V Nielsen, Michael S Cohen, Jens V Johansen, Benny R Winther, Leif R Lund, Ole Winther, Jack Taunton, Steen H Hansen, Morten Frödin

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Resumé

Udgivelsesdato: 2009-Aug-28
OriginalsprogEngelsk
TidsskriftMolecular Cell
Vol/bind35
Udgave nummer4
Sider (fra-til)511-22
Antal sider11
ISSN1097-2765
DOI
StatusUdgivet - 28. aug. 2009
Udgivet eksterntJa

Fingeraftryk

MAP Kinase Signaling System
Epithelial Cells
Cell Movement

Citer dette

Doehn, Ulrik ; Hauge, Camilla ; Frank, Scott R ; Jensen, Claus J ; Duda, Katarzyna ; Nielsen, Jakob V ; Cohen, Michael S ; Johansen, Jens V ; Winther, Benny R ; Lund, Leif R ; Winther, Ole ; Taunton, Jack ; Hansen, Steen H ; Frödin, Morten. / RSK is a principal effector of the RAS-ERK pathway for eliciting a coordinate promotile/invasive gene program and phenotype in epithelial cells. I: Molecular Cell. 2009 ; Bind 35, Nr. 4. s. 511-22.
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title = "RSK is a principal effector of the RAS-ERK pathway for eliciting a coordinate promotile/invasive gene program and phenotype in epithelial cells",
abstract = "The RAS-stimulated RAF-MEK-ERK pathway confers epithelial cells with critical motile and invasive capacities during development, tissue regeneration, and carcinoma progression, often via promoting the epithelial-mesenchymal transition (EMT). Many mechanisms by which ERK exerts this control remain elusive. We demonstrate that the ERK-activated kinase RSK is necessary to induce mesenchymal motility and invasive capacities in nontransformed epithelial and carcinoma cells. RSK is sufficient to induce certain motile responses. Expression profiling analysis revealed that a primary role of RSK is to induce transcription of a potent promotile/invasive gene program by FRA1-dependent and -independent mechanisms. The program enables RSK to coordinately modulate the extracellular environment, the intracellular motility apparatus, and receptors mediating communication between these compartments to stimulate motility and invasion. These findings uncover a mechanism whereby the RAS-ERK pathway controls epithelial cell motility by identifying RSK as a key effector, from which emanate multiple highly coordinate transcription-dependent mechanisms for stimulation of motility and invasive properties.",
author = "Ulrik Doehn and Camilla Hauge and Frank, {Scott R} and Jensen, {Claus J} and Katarzyna Duda and Nielsen, {Jakob V} and Cohen, {Michael S} and Johansen, {Jens V} and Winther, {Benny R} and Lund, {Leif R} and Ole Winther and Jack Taunton and Hansen, {Steen H} and Morten Fr{\"o}din",
year = "2009",
month = "8",
day = "28",
doi = "10.1016/j.molcel.2009.08.002",
language = "English",
volume = "35",
pages = "511--22",
journal = "Molecular Cell",
issn = "1097-2765",
publisher = "Cell Press",
number = "4",

}

Doehn, U, Hauge, C, Frank, SR, Jensen, CJ, Duda, K, Nielsen, JV, Cohen, MS, Johansen, JV, Winther, BR, Lund, LR, Winther, O, Taunton, J, Hansen, SH & Frödin, M 2009, 'RSK is a principal effector of the RAS-ERK pathway for eliciting a coordinate promotile/invasive gene program and phenotype in epithelial cells', Molecular Cell, bind 35, nr. 4, s. 511-22. https://doi.org/10.1016/j.molcel.2009.08.002

RSK is a principal effector of the RAS-ERK pathway for eliciting a coordinate promotile/invasive gene program and phenotype in epithelial cells. / Doehn, Ulrik; Hauge, Camilla; Frank, Scott R; Jensen, Claus J; Duda, Katarzyna; Nielsen, Jakob V; Cohen, Michael S; Johansen, Jens V; Winther, Benny R; Lund, Leif R; Winther, Ole; Taunton, Jack; Hansen, Steen H; Frödin, Morten.

I: Molecular Cell, Bind 35, Nr. 4, 28.08.2009, s. 511-22.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

TY - JOUR

T1 - RSK is a principal effector of the RAS-ERK pathway for eliciting a coordinate promotile/invasive gene program and phenotype in epithelial cells

AU - Doehn, Ulrik

AU - Hauge, Camilla

AU - Frank, Scott R

AU - Jensen, Claus J

AU - Duda, Katarzyna

AU - Nielsen, Jakob V

AU - Cohen, Michael S

AU - Johansen, Jens V

AU - Winther, Benny R

AU - Lund, Leif R

AU - Winther, Ole

AU - Taunton, Jack

AU - Hansen, Steen H

AU - Frödin, Morten

PY - 2009/8/28

Y1 - 2009/8/28

N2 - The RAS-stimulated RAF-MEK-ERK pathway confers epithelial cells with critical motile and invasive capacities during development, tissue regeneration, and carcinoma progression, often via promoting the epithelial-mesenchymal transition (EMT). Many mechanisms by which ERK exerts this control remain elusive. We demonstrate that the ERK-activated kinase RSK is necessary to induce mesenchymal motility and invasive capacities in nontransformed epithelial and carcinoma cells. RSK is sufficient to induce certain motile responses. Expression profiling analysis revealed that a primary role of RSK is to induce transcription of a potent promotile/invasive gene program by FRA1-dependent and -independent mechanisms. The program enables RSK to coordinately modulate the extracellular environment, the intracellular motility apparatus, and receptors mediating communication between these compartments to stimulate motility and invasion. These findings uncover a mechanism whereby the RAS-ERK pathway controls epithelial cell motility by identifying RSK as a key effector, from which emanate multiple highly coordinate transcription-dependent mechanisms for stimulation of motility and invasive properties.

AB - The RAS-stimulated RAF-MEK-ERK pathway confers epithelial cells with critical motile and invasive capacities during development, tissue regeneration, and carcinoma progression, often via promoting the epithelial-mesenchymal transition (EMT). Many mechanisms by which ERK exerts this control remain elusive. We demonstrate that the ERK-activated kinase RSK is necessary to induce mesenchymal motility and invasive capacities in nontransformed epithelial and carcinoma cells. RSK is sufficient to induce certain motile responses. Expression profiling analysis revealed that a primary role of RSK is to induce transcription of a potent promotile/invasive gene program by FRA1-dependent and -independent mechanisms. The program enables RSK to coordinately modulate the extracellular environment, the intracellular motility apparatus, and receptors mediating communication between these compartments to stimulate motility and invasion. These findings uncover a mechanism whereby the RAS-ERK pathway controls epithelial cell motility by identifying RSK as a key effector, from which emanate multiple highly coordinate transcription-dependent mechanisms for stimulation of motility and invasive properties.

U2 - 10.1016/j.molcel.2009.08.002

DO - 10.1016/j.molcel.2009.08.002

M3 - Journal article

VL - 35

SP - 511

EP - 522

JO - Molecular Cell

JF - Molecular Cell

SN - 1097-2765

IS - 4

ER -