Polarized NHE1 and SWELL1 regulate migration direction, efficiency and metastasis

Cell migration regulates diverse (patho)physiological processes, including cancer metastasis. According to the Osmotic Engine Model, polarization of NHE1 at the leading edge of confined cells facilitates water uptake, cell protrusion and motility. The physiological relevance of the Osmotic Engine Mo...

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Published inNature communications Vol. 13; no. 1; pp. 6128 - 17
Main Authors Zhang, Yuqi, Li, Yizeng, Thompson, Keyata N, Stoletov, Konstantin, Yuan, Qinling, Bera, Kaustav, Lee, Se Jong, Zhao, Runchen, Kiepas, Alexander, Wang, Yao, Mistriotis, Panagiotis, Serra, Selma A, Lewis, John D, Valverde, Miguel A, Martin, Stuart S, Sun, Sean X, Konstantopoulos, Konstantinos
Format Journal Article
LanguageEnglish
Published England Nature Publishing Group 17.10.2022
Nature Publishing Group UK
Nature Portfolio
Subjects
Breast cancer
Cancer
Cdc42 protein
Cell activation
Cell adhesion & migration
Cell migration
Cell Movement - physiology
Cell Size
Chloride ions
Extravasation
Humans
Ion channels
Ion exchangers
Leading edges
Metastases
Metastasis
Neoplasms
Physiology
Polarization
RhoA protein
Sodium-Hydrogen Exchangers
Spheroids
Trailing edges
Water
Water uptake
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Abstract Cell migration regulates diverse (patho)physiological processes, including cancer metastasis. According to the Osmotic Engine Model, polarization of NHE1 at the leading edge of confined cells facilitates water uptake, cell protrusion and motility. The physiological relevance of the Osmotic Engine Model and the identity of molecules mediating cell rear shrinkage remain elusive. Here, we demonstrate that NHE1 and SWELL1 preferentially polarize at the cell leading and trailing edges, respectively, mediate cell volume regulation, cell dissemination from spheroids and confined migration. SWELL1 polarization confers migration direction and efficiency, as predicted mathematically and determined experimentally via optogenetic spatiotemporal regulation. Optogenetic RhoA activation at the cell front triggers SWELL1 re-distribution and migration direction reversal in SWELL1-expressing, but not SWELL1-knockdown, cells. Efficient cell reversal also requires Cdc42, which controls NHE1 repolarization. Dual NHE1/SWELL1 knockdown inhibits breast cancer cell extravasation and metastasis in vivo, thereby illustrating the physiological significance of the Osmotic Engine Model.
AbstractList Cell migration regulates diverse (patho)physiological processes, including cancer metastasis. According to the Osmotic Engine Model, polarization of NHE1 at the leading edge of confined cells facilitates water uptake, cell protrusion and motility. The physiological relevance of the Osmotic Engine Model and the identity of molecules mediating cell rear shrinkage remain elusive. Here, we demonstrate that NHE1 and SWELL1 preferentially polarize at the cell leading and trailing edges, respectively, mediate cell volume regulation, cell dissemination from spheroids and confined migration. SWELL1 polarization confers migration direction and efficiency, as predicted mathematically and determined experimentally via optogenetic spatiotemporal regulation. Optogenetic RhoA activation at the cell front triggers SWELL1 re-distribution and migration direction reversal in SWELL1-expressing, but not SWELL1-knockdown, cells. Efficient cell reversal also requires Cdc42, which controls NHE1 repolarization. Dual NHE1/SWELL1 knockdown inhibits breast cancer cell extravasation and metastasis in vivo, thereby illustrating the physiological significance of the Osmotic Engine Model. Cell migration regulates diverse (patho)physiological processes, including cancer metastasis. Here the authors show that the chloride ion channel SWELL1 and the ion exchanger NHE1 are preferentially enriched at the trailing and leading edges, respectively, of migrating cells and regulate cell volume to propel confined cells, favouring breast cancer cell extravasation and metastasis.
Cell migration regulates diverse (patho)physiological processes, including cancer metastasis. Here the authors show that the chloride ion channel SWELL1 and the ion exchanger NHE1 are preferentially enriched at the trailing and leading edges, respectively, of migrating cells and regulate cell volume to propel confined cells, favouring breast cancer cell extravasation and metastasis.
Cell migration regulates diverse (patho)physiological processes, including cancer metastasis. According to the Osmotic Engine Model, polarization of NHE1 at the leading edge of confined cells facilitates water uptake, cell protrusion and motility. The physiological relevance of the Osmotic Engine Model and the identity of molecules mediating cell rear shrinkage remain elusive. Here, we demonstrate that NHE1 and SWELL1 preferentially polarize at the cell leading and trailing edges, respectively, mediate cell volume regulation, cell dissemination from spheroids and confined migration. SWELL1 polarization confers migration direction and efficiency, as predicted mathematically and determined experimentally via optogenetic spatiotemporal regulation. Optogenetic RhoA activation at the cell front triggers SWELL1 re-distribution and migration direction reversal in SWELL1-expressing, but not SWELL1-knockdown, cells. Efficient cell reversal also requires Cdc42, which controls NHE1 repolarization. Dual NHE1/SWELL1 knockdown inhibits breast cancer cell extravasation and metastasis in vivo, thereby illustrating the physiological significance of the Osmotic Engine Model.
Cell migration regulates diverse (patho)physiological processes, including cancer metastasis. According to the Osmotic Engine Model, polarization of NHE1 at the leading edge of confined cells facilitates water uptake, cell protrusion and motility. The physiological relevance of the Osmotic Engine Model and the identity of molecules mediating cell rear shrinkage remain elusive. Here, we demonstrate that NHE1 and SWELL1 preferentially polarize at the cell leading and trailing edges, respectively, mediate cell volume regulation, cell dissemination from spheroids and confined migration. SWELL1 polarization confers migration direction and efficiency, as predicted mathematically and determined experimentally via optogenetic spatiotemporal regulation. Optogenetic RhoA activation at the cell front triggers SWELL1 re-distribution and migration direction reversal in SWELL1-expressing, but not SWELL1-knockdown, cells. Efficient cell reversal also requires Cdc42, which controls NHE1 repolarization. Dual NHE1/SWELL1 knockdown inhibits breast cancer cell extravasation and metastasis in vivo, thereby illustrating the physiological significance of the Osmotic Engine Model.Cell migration regulates diverse (patho)physiological processes, including cancer metastasis. Here the authors show that the chloride ion channel SWELL1 and the ion exchanger NHE1 are preferentially enriched at the trailing and leading edges, respectively, of migrating cells and regulate cell volume to propel confined cells, favouring breast cancer cell extravasation and metastasis.
Abstract Cell migration regulates diverse (patho)physiological processes, including cancer metastasis. According to the Osmotic Engine Model, polarization of NHE1 at the leading edge of confined cells facilitates water uptake, cell protrusion and motility. The physiological relevance of the Osmotic Engine Model and the identity of molecules mediating cell rear shrinkage remain elusive. Here, we demonstrate that NHE1 and SWELL1 preferentially polarize at the cell leading and trailing edges, respectively, mediate cell volume regulation, cell dissemination from spheroids and confined migration. SWELL1 polarization confers migration direction and efficiency, as predicted mathematically and determined experimentally via optogenetic spatiotemporal regulation. Optogenetic RhoA activation at the cell front triggers SWELL1 re-distribution and migration direction reversal in SWELL1-expressing, but not SWELL1-knockdown, cells. Efficient cell reversal also requires Cdc42, which controls NHE1 repolarization. Dual NHE1/SWELL1 knockdown inhibits breast cancer cell extravasation and metastasis in vivo, thereby illustrating the physiological significance of the Osmotic Engine Model.
Cell migration regulates diverse (patho)physiological processes, including cancer metastasis. According to the Osmotic Engine Model, polarization of NHE1 at the leading edge of confined cells facilitates water uptake, cell protrusion and motility. The physiological relevance of the Osmotic Engine Model and the identity of molecules mediating cell rear shrinkage remain elusive. Here, we demonstrate that NHE1 and SWELL1 preferentially polarize at the cell leading and trailing edges, respectively, mediate cell volume regulation, cell dissemination from spheroids and confined migration. SWELL1 polarization confers migration direction and efficiency, as predicted mathematically and determined experimentally via optogenetic spatiotemporal regulation. Optogenetic RhoA activation at the cell front triggers SWELL1 re-distribution and migration direction reversal in SWELL1-expressing, but not SWELL1-knockdown, cells. Efficient cell reversal also requires Cdc42, which controls NHE1 repolarization. Dual NHE1/SWELL1 knockdown inhibits breast cancer cell extravasation and metastasis in vivo, thereby illustrating the physiological significance of the Osmotic Engine Model.Cell migration regulates diverse (patho)physiological processes, including cancer metastasis. According to the Osmotic Engine Model, polarization of NHE1 at the leading edge of confined cells facilitates water uptake, cell protrusion and motility. The physiological relevance of the Osmotic Engine Model and the identity of molecules mediating cell rear shrinkage remain elusive. Here, we demonstrate that NHE1 and SWELL1 preferentially polarize at the cell leading and trailing edges, respectively, mediate cell volume regulation, cell dissemination from spheroids and confined migration. SWELL1 polarization confers migration direction and efficiency, as predicted mathematically and determined experimentally via optogenetic spatiotemporal regulation. Optogenetic RhoA activation at the cell front triggers SWELL1 re-distribution and migration direction reversal in SWELL1-expressing, but not SWELL1-knockdown, cells. Efficient cell reversal also requires Cdc42, which controls NHE1 repolarization. Dual NHE1/SWELL1 knockdown inhibits breast cancer cell extravasation and metastasis in vivo, thereby illustrating the physiological significance of the Osmotic Engine Model.
ArticleNumber 6128
Author Serra, Selma A
Zhang, Yuqi
Yuan, Qinling
Martin, Stuart S
Zhao, Runchen
Sun, Sean X
Stoletov, Konstantin
Wang, Yao
Mistriotis, Panagiotis
Konstantopoulos, Konstantinos
Lee, Se Jong
Kiepas, Alexander
Valverde, Miguel A
Thompson, Keyata N
Lewis, John D
Bera, Kaustav
Li, Yizeng
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Cites_doi 10.1103/PhysRevLett.115.268101
10.1096/fj.12-211441
10.1126/sciadv.aaw7243
10.1038/nrm.2016.29
10.1038/nrm2820
10.1152/physrev.00018.2011
10.1083/jcb.201302132
10.1126/science.aau3301
10.1096/fj.12-203786
10.1016/j.cell.2014.03.024
10.1038/ncb1019
10.1126/sciadv.abh3457
10.1038/srep42088
10.1038/nrc.2016.123
10.1073/pnas.1907625116
10.1073/pnas.2025013118
10.1083/jcb.201902057
10.1038/s41556-017-0012-0
10.1016/j.bpj.2018.04.045
10.1152/ajpcell.00038.2001
10.1021/acs.nanolett.8b04720
10.1111/j.1748-1716.2006.01558.x
10.1038/ncomms14396
10.1016/j.ceb.2015.08.005
10.1126/sciadv.aba6505
10.1016/j.cell.2011.11.016
10.1159/000368521
10.1007/978-1-4939-3801-8_3
10.1586/14737140.2015.1058711
10.1007/s10549-016-4013-7
10.1007/s12013-012-9340-7
10.1038/s41467-019-14160-8
10.1016/j.cell.2014.02.052
10.1016/j.celrep.2016.04.035
10.1038/315063a0
10.1038/355830a0
10.1007/s00424-013-1293-1
10.1126/science.1252826
10.18632/oncotarget.6159
10.1016/j.cell.2013.11.029
10.1007/s10120-021-01187-4
10.1242/jcs.240341
10.1158/0008-5472.CAN-18-3369
10.18632/oncoscience.27
10.1016/j.cell.2015.01.007
10.1016/j.ceb.2014.06.001
10.1126/sciadv.abg4934
10.3390/ijms20112663
10.1091/mbc.7.9.1419
10.1016/j.ebiom.2019.09.007
10.5281/zenodo.7105392
10.1038/s41551-019-0400-9
10.3389/fcell.2021.683686
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References V Pang (33683_CR52) 2012; 63
DC Gadsby (33683_CR48) 1985; 315
Z Qiu (33683_CR8) 2014; 157
KM Stroka (33683_CR6) 2014; 30
MA Valverde (33683_CR42) 1992; 355
YJ Liu (33683_CR21) 2015; 160
WC Hung (33683_CR36) 2013; 202
MR Dallas (33683_CR28) 2012; 26
KN Thompson (33683_CR13) 2015; 6
I Carton (33683_CR24) 2002; 283
E Sahai (33683_CR23) 2003; 5
L Valon (33683_CR17) 2017; 8
EO Wisniewski (33683_CR22) 2020; 6
WC Hung (33683_CR37) 2016; 15
33683_CR27
K Kurashima (33683_CR33) 2021; 24
KM Stroka (33683_CR7) 2014; 157
P Mistriotis (33683_CR10) 2019; 218
BS Wong (33683_CR38) 2019; 79
R Zhao (33683_CR39) 2019; 5
S Dadakhujaev (33683_CR40) 2014; 1
P Lu (33683_CR32) 2019; 48
FK Voss (33683_CR9) 2014; 344
RT Alexander (33683_CR50) 2006; 187
A Schwab (33683_CR5) 2012; 92
SP Carey (33683_CR14) 2017; 7
33683_CR35
33683_CR34
Y Li (33683_CR47) 2015; 115
Y Li (33683_CR16) 2019; 116
CD Paul (33683_CR2) 2017; 17
PG Valles (33683_CR46) 2015; 40
BC Tilly (33683_CR25) 1996; 7
KJ Cheung (33683_CR41) 2013; 155
S van Helvert (33683_CR3) 2018; 20
A Bueno-Orovio (33683_CR49) 2014; 466
Y Li (33683_CR15) 2018; 114
EM Balzer (33683_CR19) 2012; 26
L Willetts (33683_CR30) 2016; 1458
33683_CR44
AW Holle (33683_CR20) 2019; 19
A Lanczky (33683_CR31) 2016; 160
W Deng (33683_CR43) 2020; 11
TJ Jentsch (33683_CR4) 2016; 17
JR Casey (33683_CR51) 2010; 11
P Friedl (33683_CR1) 2011; 147
A Shellard (33683_CR18) 2018; 362
CL Yankaskas (33683_CR12) 2019; 3
K Stoletov (33683_CR29) 2015; 15
AJ Ridley (33683_CR26) 2015; 36
33683_CR53
33683_CR11
Y Li (33683_CR45) 2021; 9
References_xml – volume: 115
  start-page: 268101
  year: 2015
  ident: 33683_CR47
  publication-title: Phys. Rev. Lett.
  doi: 10.1103/PhysRevLett.115.268101
  contributor:
    fullname: Y Li
– volume: 26
  start-page: 4045
  year: 2012
  ident: 33683_CR19
  publication-title: FASEB J.
  doi: 10.1096/fj.12-211441
  contributor:
    fullname: EM Balzer
– volume: 5
  start-page: eaaw7243
  year: 2019
  ident: 33683_CR39
  publication-title: Sci. Adv.
  doi: 10.1126/sciadv.aaw7243
  contributor:
    fullname: R Zhao
– volume: 17
  start-page: 293
  year: 2016
  ident: 33683_CR4
  publication-title: Nat. Rev. Mol. Cell Biol.
  doi: 10.1038/nrm.2016.29
  contributor:
    fullname: TJ Jentsch
– volume: 11
  start-page: 50
  year: 2010
  ident: 33683_CR51
  publication-title: Nat. Rev. Mol. Cell Biol.
  doi: 10.1038/nrm2820
  contributor:
    fullname: JR Casey
– volume: 92
  start-page: 1865
  year: 2012
  ident: 33683_CR5
  publication-title: Physiol. Rev.
  doi: 10.1152/physrev.00018.2011
  contributor:
    fullname: A Schwab
– volume: 202
  start-page: 807
  year: 2013
  ident: 33683_CR36
  publication-title: J. Cell Biol.
  doi: 10.1083/jcb.201302132
  contributor:
    fullname: WC Hung
– volume: 362
  start-page: 339
  year: 2018
  ident: 33683_CR18
  publication-title: Science
  doi: 10.1126/science.aau3301
  contributor:
    fullname: A Shellard
– volume: 26
  start-page: 2648
  year: 2012
  ident: 33683_CR28
  publication-title: FASEB J.
  doi: 10.1096/fj.12-203786
  contributor:
    fullname: MR Dallas
– volume: 157
  start-page: 447
  year: 2014
  ident: 33683_CR8
  publication-title: Cell
  doi: 10.1016/j.cell.2014.03.024
  contributor:
    fullname: Z Qiu
– volume: 5
  start-page: 711
  year: 2003
  ident: 33683_CR23
  publication-title: Nat. Cell Biol.
  doi: 10.1038/ncb1019
  contributor:
    fullname: E Sahai
– ident: 33683_CR27
  doi: 10.1126/sciadv.abh3457
– volume: 7
  year: 2017
  ident: 33683_CR14
  publication-title: Sci. Rep.
  doi: 10.1038/srep42088
  contributor:
    fullname: SP Carey
– volume: 17
  start-page: 131
  year: 2017
  ident: 33683_CR2
  publication-title: Nat. Rev. Cancer
  doi: 10.1038/nrc.2016.123
  contributor:
    fullname: CD Paul
– volume: 116
  start-page: 23894
  year: 2019
  ident: 33683_CR16
  publication-title: Proc. Natl Acad. Sci. USA
  doi: 10.1073/pnas.1907625116
  contributor:
    fullname: Y Li
– ident: 33683_CR35
  doi: 10.1073/pnas.2025013118
– volume: 218
  start-page: 4093
  year: 2019
  ident: 33683_CR10
  publication-title: J. Cell Biol.
  doi: 10.1083/jcb.201902057
  contributor:
    fullname: P Mistriotis
– volume: 20
  start-page: 8
  year: 2018
  ident: 33683_CR3
  publication-title: Nat. Cell Biol.
  doi: 10.1038/s41556-017-0012-0
  contributor:
    fullname: S van Helvert
– volume: 114
  start-page: 2965
  year: 2018
  ident: 33683_CR15
  publication-title: Biophys. J.
  doi: 10.1016/j.bpj.2018.04.045
  contributor:
    fullname: Y Li
– volume: 283
  start-page: C115
  year: 2002
  ident: 33683_CR24
  publication-title: Am. J. Physiol. Cell Physiol.
  doi: 10.1152/ajpcell.00038.2001
  contributor:
    fullname: I Carton
– volume: 19
  start-page: 2280
  year: 2019
  ident: 33683_CR20
  publication-title: Nano Lett.
  doi: 10.1021/acs.nanolett.8b04720
  contributor:
    fullname: AW Holle
– volume: 187
  start-page: 159
  year: 2006
  ident: 33683_CR50
  publication-title: Acta Physiol. (Oxf.)
  doi: 10.1111/j.1748-1716.2006.01558.x
  contributor:
    fullname: RT Alexander
– volume: 8
  year: 2017
  ident: 33683_CR17
  publication-title: Nat. Commun.
  doi: 10.1038/ncomms14396
  contributor:
    fullname: L Valon
– volume: 36
  start-page: 103
  year: 2015
  ident: 33683_CR26
  publication-title: Curr. Opin. Cell Biol.
  doi: 10.1016/j.ceb.2015.08.005
  contributor:
    fullname: AJ Ridley
– volume: 6
  start-page: eaba6505
  year: 2020
  ident: 33683_CR22
  publication-title: Sci. Adv.
  doi: 10.1126/sciadv.aba6505
  contributor:
    fullname: EO Wisniewski
– volume: 147
  start-page: 992
  year: 2011
  ident: 33683_CR1
  publication-title: Cell
  doi: 10.1016/j.cell.2011.11.016
  contributor:
    fullname: P Friedl
– volume: 40
  start-page: 452
  year: 2015
  ident: 33683_CR46
  publication-title: Kidney Blood Press Res.
  doi: 10.1159/000368521
  contributor:
    fullname: PG Valles
– volume: 1458
  start-page: 27
  year: 2016
  ident: 33683_CR30
  publication-title: Methods Mol. Biol.
  doi: 10.1007/978-1-4939-3801-8_3
  contributor:
    fullname: L Willetts
– volume: 15
  start-page: 733
  year: 2015
  ident: 33683_CR29
  publication-title: Expert Rev. Anticancer Ther.
  doi: 10.1586/14737140.2015.1058711
  contributor:
    fullname: K Stoletov
– volume: 160
  start-page: 439
  year: 2016
  ident: 33683_CR31
  publication-title: Breast Cancer Res. Treat.
  doi: 10.1007/s10549-016-4013-7
  contributor:
    fullname: A Lanczky
– volume: 63
  start-page: 47
  year: 2012
  ident: 33683_CR52
  publication-title: Cell Biochem. Biophys.
  doi: 10.1007/s12013-012-9340-7
  contributor:
    fullname: V Pang
– volume: 11
  year: 2020
  ident: 33683_CR43
  publication-title: Nat. Commun.
  doi: 10.1038/s41467-019-14160-8
  contributor:
    fullname: W Deng
– volume: 157
  start-page: 611
  year: 2014
  ident: 33683_CR7
  publication-title: Cell
  doi: 10.1016/j.cell.2014.02.052
  contributor:
    fullname: KM Stroka
– volume: 15
  start-page: 1430
  year: 2016
  ident: 33683_CR37
  publication-title: Cell Rep.
  doi: 10.1016/j.celrep.2016.04.035
  contributor:
    fullname: WC Hung
– volume: 315
  start-page: 63
  year: 1985
  ident: 33683_CR48
  publication-title: Nature
  doi: 10.1038/315063a0
  contributor:
    fullname: DC Gadsby
– volume: 355
  start-page: 830
  year: 1992
  ident: 33683_CR42
  publication-title: Nature
  doi: 10.1038/355830a0
  contributor:
    fullname: MA Valverde
– volume: 466
  start-page: 183
  year: 2014
  ident: 33683_CR49
  publication-title: Pflug. Arch.
  doi: 10.1007/s00424-013-1293-1
  contributor:
    fullname: A Bueno-Orovio
– volume: 344
  start-page: 634
  year: 2014
  ident: 33683_CR9
  publication-title: Science
  doi: 10.1126/science.1252826
  contributor:
    fullname: FK Voss
– volume: 6
  start-page: 35231
  year: 2015
  ident: 33683_CR13
  publication-title: Oncotarget
  doi: 10.18632/oncotarget.6159
  contributor:
    fullname: KN Thompson
– volume: 155
  start-page: 1639
  year: 2013
  ident: 33683_CR41
  publication-title: Cell
  doi: 10.1016/j.cell.2013.11.029
  contributor:
    fullname: KJ Cheung
– volume: 24
  start-page: 1063
  year: 2021
  ident: 33683_CR33
  publication-title: Gastric Cancer
  doi: 10.1007/s10120-021-01187-4
  contributor:
    fullname: K Kurashima
– ident: 33683_CR44
  doi: 10.1242/jcs.240341
– volume: 79
  start-page: 2878
  year: 2019
  ident: 33683_CR38
  publication-title: Cancer Res.
  doi: 10.1158/0008-5472.CAN-18-3369
  contributor:
    fullname: BS Wong
– volume: 1
  start-page: 229
  year: 2014
  ident: 33683_CR40
  publication-title: Oncoscience
  doi: 10.18632/oncoscience.27
  contributor:
    fullname: S Dadakhujaev
– volume: 160
  start-page: 659
  year: 2015
  ident: 33683_CR21
  publication-title: Cell
  doi: 10.1016/j.cell.2015.01.007
  contributor:
    fullname: YJ Liu
– volume: 30
  start-page: 41
  year: 2014
  ident: 33683_CR6
  publication-title: Curr. Opin. Cell Biol.
  doi: 10.1016/j.ceb.2014.06.001
  contributor:
    fullname: KM Stroka
– ident: 33683_CR11
  doi: 10.1126/sciadv.abg4934
– ident: 33683_CR34
  doi: 10.3390/ijms20112663
– volume: 7
  start-page: 1419
  year: 1996
  ident: 33683_CR25
  publication-title: Mol. Biol. Cell
  doi: 10.1091/mbc.7.9.1419
  contributor:
    fullname: BC Tilly
– volume: 48
  start-page: 100
  year: 2019
  ident: 33683_CR32
  publication-title: EBioMedicine
  doi: 10.1016/j.ebiom.2019.09.007
  contributor:
    fullname: P Lu
– ident: 33683_CR53
  doi: 10.5281/zenodo.7105392
– volume: 3
  start-page: 452
  year: 2019
  ident: 33683_CR12
  publication-title: Nat. Biomed. Eng.
  doi: 10.1038/s41551-019-0400-9
  contributor:
    fullname: CL Yankaskas
– volume: 9
  start-page: 683686
  year: 2021
  ident: 33683_CR45
  publication-title: Front. Cell Dev. Biol.
  doi: 10.3389/fcell.2021.683686
  contributor:
    fullname: Y Li
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Snippet Cell migration regulates diverse (patho)physiological processes, including cancer metastasis. According to the Osmotic Engine Model, polarization of NHE1 at...
Abstract Cell migration regulates diverse (patho)physiological processes, including cancer metastasis. According to the Osmotic Engine Model, polarization of...
Cell migration regulates diverse (patho)physiological processes, including cancer metastasis. Here the authors show that the chloride ion channel SWELL1 and...
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StartPage 6128
SubjectTerms Breast cancer
Cancer
Cdc42 protein
Cell activation
Cell adhesion & migration
Cell migration
Cell Movement - physiology
Cell Size
Chloride ions
Extravasation
Humans
Ion channels
Ion exchangers
Leading edges
Metastases
Metastasis
Neoplasms
Physiology
Polarization
RhoA protein
Sodium-Hydrogen Exchangers
Spheroids
Trailing edges
Water
Water uptake
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Title Polarized NHE1 and SWELL1 regulate migration direction, efficiency and metastasis
URI https://www.ncbi.nlm.nih.gov/pubmed/36253369
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https://pubmed.ncbi.nlm.nih.gov/PMC9576788
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