MT1-MMP targeting to endolysosomes is mediated by upregulation of flotillins

Damien Planchon; Eduardo Rios Morris; Mallory Genest; Franck Comunale; Sophie Vacher; Ivan Bièche; Evgeny V Denisov; Lubov A Tashireva; Vladimir M Perelmuter; Stefan Linder; Philippe Chavrier; Stéphane Bodin; Cécile Gauthier-Rouvière

doi:10.1242/jcs.218925

MT1-MMP targeting to endolysosomes is mediated by upregulation of flotillins

Standard

MT1-MMP targeting to endolysosomes is mediated by upregulation of flotillins. / Planchon, Damien; Rios Morris, Eduardo; Genest, Mallory; Comunale, Franck; Vacher, Sophie; Bièche, Ivan; Denisov, Evgeny V; Tashireva, Lubov A; Perelmuter, Vladimir M; Linder, Stefan; Chavrier, Philippe; Bodin, Stéphane; Gauthier-Rouvière, Cécile.

in: J CELL SCI, Jahrgang 131, Nr. 17, 05.09.2018, S. jcs218925.

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

Harvard

Planchon, D, Rios Morris, E, Genest, M, Comunale, F, Vacher, S, Bièche, I, Denisov, EV, Tashireva, LA, Perelmuter, VM, Linder, S, Chavrier, P, Bodin, S & Gauthier-Rouvière, C 2018, 'MT1-MMP targeting to endolysosomes is mediated by upregulation of flotillins', J CELL SCI, Jg. 131, Nr. 17, S. jcs218925. https://doi.org/10.1242/jcs.218925

APA

Planchon, D., Rios Morris, E., Genest, M., Comunale, F., Vacher, S., Bièche, I., Denisov, E. V., Tashireva, L. A., Perelmuter, V. M., Linder, S., Chavrier, P., Bodin, S., & Gauthier-Rouvière, C. (2018). MT1-MMP targeting to endolysosomes is mediated by upregulation of flotillins. J CELL SCI, 131(17), jcs218925. https://doi.org/10.1242/jcs.218925

Vancouver

Planchon D, Rios Morris E, Genest M, Comunale F, Vacher S, Bièche I et al. MT1-MMP targeting to endolysosomes is mediated by upregulation of flotillins. J CELL SCI. 2018 Sep 5;131(17):jcs218925. https://doi.org/10.1242/jcs.218925

Bibtex

@article{1c96d158ee124ce88629d9ccc427e725,

title = "MT1-MMP targeting to endolysosomes is mediated by upregulation of flotillins",

abstract = "Tumor cell invasion and metastasis formation are the major cause of death in cancer patients. These processes rely on extracellular matrix (ECM) degradation mediated by organelles termed invadopodia, to which the transmembrane matrix metalloproteinase MT1-MMP (also known as MMP14) is delivered from its reservoir, the RAB7-containing endolysosomes. How MT1-MMP is targeted to endolysosomes remains to be elucidated. Flotillin-1 and -2 are upregulated in many invasive cancers. Here, we show that flotillin upregulation triggers a general mechanism, common to carcinoma and sarcoma, which promotes RAB5-dependent MT1-MMP endocytosis and its delivery to RAB7-positive endolysosomal reservoirs. Conversely, flotillin knockdown in invasive cancer cells greatly reduces MT1-MMP accumulation in endolysosomes, its subsequent exocytosis at invadopodia, ECM degradation and cell invasion. Our results demonstrate that flotillin upregulation is necessary and sufficient to promote epithelial and mesenchymal cancer cell invasion and ECM degradation by controlling MT1-MMP endocytosis and delivery to the endolysosomal recycling compartment.",

keywords = "Journal Article",

author = "Damien Planchon and {Rios Morris}, Eduardo and Mallory Genest and Franck Comunale and Sophie Vacher and Ivan Bi{\`e}che and Denisov, {Evgeny V} and Tashireva, {Lubov A} and Perelmuter, {Vladimir M} and Stefan Linder and Philippe Chavrier and St{\'e}phane Bodin and C{\'e}cile Gauthier-Rouvi{\`e}re",

note = "{\textcopyright} 2018. Published by The Company of Biologists Ltd.",

year = "2018",

month = sep,

day = "5",

doi = "10.1242/jcs.218925",

language = "English",

volume = "131",

pages = "jcs218925",

journal = "J CELL SCI",

issn = "0021-9533",

publisher = "Company of Biologists Ltd",

number = "17",

}

RIS

TY - JOUR

T1 - MT1-MMP targeting to endolysosomes is mediated by upregulation of flotillins

AU - Planchon, Damien

AU - Rios Morris, Eduardo

AU - Genest, Mallory

AU - Comunale, Franck

AU - Vacher, Sophie

AU - Bièche, Ivan

AU - Denisov, Evgeny V

AU - Tashireva, Lubov A

AU - Perelmuter, Vladimir M

AU - Linder, Stefan

AU - Chavrier, Philippe

AU - Bodin, Stéphane

AU - Gauthier-Rouvière, Cécile

PY - 2018/9/5

Y1 - 2018/9/5

N2 - Tumor cell invasion and metastasis formation are the major cause of death in cancer patients. These processes rely on extracellular matrix (ECM) degradation mediated by organelles termed invadopodia, to which the transmembrane matrix metalloproteinase MT1-MMP (also known as MMP14) is delivered from its reservoir, the RAB7-containing endolysosomes. How MT1-MMP is targeted to endolysosomes remains to be elucidated. Flotillin-1 and -2 are upregulated in many invasive cancers. Here, we show that flotillin upregulation triggers a general mechanism, common to carcinoma and sarcoma, which promotes RAB5-dependent MT1-MMP endocytosis and its delivery to RAB7-positive endolysosomal reservoirs. Conversely, flotillin knockdown in invasive cancer cells greatly reduces MT1-MMP accumulation in endolysosomes, its subsequent exocytosis at invadopodia, ECM degradation and cell invasion. Our results demonstrate that flotillin upregulation is necessary and sufficient to promote epithelial and mesenchymal cancer cell invasion and ECM degradation by controlling MT1-MMP endocytosis and delivery to the endolysosomal recycling compartment.

AB - Tumor cell invasion and metastasis formation are the major cause of death in cancer patients. These processes rely on extracellular matrix (ECM) degradation mediated by organelles termed invadopodia, to which the transmembrane matrix metalloproteinase MT1-MMP (also known as MMP14) is delivered from its reservoir, the RAB7-containing endolysosomes. How MT1-MMP is targeted to endolysosomes remains to be elucidated. Flotillin-1 and -2 are upregulated in many invasive cancers. Here, we show that flotillin upregulation triggers a general mechanism, common to carcinoma and sarcoma, which promotes RAB5-dependent MT1-MMP endocytosis and its delivery to RAB7-positive endolysosomal reservoirs. Conversely, flotillin knockdown in invasive cancer cells greatly reduces MT1-MMP accumulation in endolysosomes, its subsequent exocytosis at invadopodia, ECM degradation and cell invasion. Our results demonstrate that flotillin upregulation is necessary and sufficient to promote epithelial and mesenchymal cancer cell invasion and ECM degradation by controlling MT1-MMP endocytosis and delivery to the endolysosomal recycling compartment.

KW - Journal Article

U2 - 10.1242/jcs.218925

DO - 10.1242/jcs.218925

M3 - SCORING: Journal article

C2 - 30111578

VL - 131

SP - jcs218925

JO - J CELL SCI

JF - J CELL SCI

SN - 0021-9533

IS - 17

ER -