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

Research output: Contribution to journalJournal articlepeer-review

Standard

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 Antonio Juel; 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.

In: Molecular Cell, Vol. 35, No. 4, 2009, p. 511-22.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Doehn, U, Hauge, C, Frank, SR, Jensen, CAJ, 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, vol. 35, no. 4, pp. 511-22. https://doi.org/10.1016/j.molcel.2009.08.002

APA

Doehn, U., Hauge, C., Frank, S. R., Jensen, C. A. J., Duda, K., Nielsen, J. V., Cohen, M. S., Johansen, J. V., Winther, B. R., Lund, L. R., Winther, O., Taunton, J., Hansen, S. H., & 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, 35(4), 511-22. https://doi.org/10.1016/j.molcel.2009.08.002

Vancouver

Doehn U, Hauge C, Frank SR, Jensen CAJ, Duda K, Nielsen JV et al. 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. 2009;35(4):511-22. https://doi.org/10.1016/j.molcel.2009.08.002

Author

Doehn, Ulrik ; Hauge, Camilla ; Frank, Scott R ; Jensen, Claus Antonio Juel ; 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. In: Molecular Cell. 2009 ; Vol. 35, No. 4. pp. 511-22.

Bibtex

@article{f689b4e0d5cf11dea1f3000ea68e967b,
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 Antonio Juel} 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",
note = "Keywords: Animals; Carcinoma; Cell Line; Cell Movement; Cell Transdifferentiation; Cell Transformation, Neoplastic; Dogs; Epithelial Cells; Extracellular Signal-Regulated MAP Kinases; Gene Expression Profiling; Gene Expression Regulation, Neoplastic; Genotype; Humans; Mesoderm; Neoplasm Invasiveness; Phenotype; Proto-Oncogene Proteins c-fos; Ribosomal Protein S6 Kinases, 90-kDa; Signal Transduction; Time Factors; Transcription, Genetic; Transduction, Genetic; ras Proteins",
year = "2009",
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",

}

RIS

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 Antonio Juel

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

N1 - Keywords: Animals; Carcinoma; Cell Line; Cell Movement; Cell Transdifferentiation; Cell Transformation, Neoplastic; Dogs; Epithelial Cells; Extracellular Signal-Regulated MAP Kinases; Gene Expression Profiling; Gene Expression Regulation, Neoplastic; Genotype; Humans; Mesoderm; Neoplasm Invasiveness; Phenotype; Proto-Oncogene Proteins c-fos; Ribosomal Protein S6 Kinases, 90-kDa; Signal Transduction; Time Factors; Transcription, Genetic; Transduction, Genetic; ras Proteins

PY - 2009

Y1 - 2009

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

C2 - 19716794

VL - 35

SP - 511

EP - 522

JO - Molecular Cell

JF - Molecular Cell

SN - 1097-2765

IS - 4

ER -

ID: 15924323