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Bone marrow-derived myofibroblasts are the providers of pro-invasive matrix metalloproteinase 13 in primary tumor

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Harvard

Lecomte, J, Masset, A, Blacher, S, Maertens, L, Gothot, A, Delgaudine, M, Bruyère, F, Carnet, O, Paupert, J, Illemann, M, Foidart, J-M, Lund, IK, Høyer-Hansen, G & Noel, A 2012, 'Bone marrow-derived myofibroblasts are the providers of pro-invasive matrix metalloproteinase 13 in primary tumor' Neoplasia, bind 14, nr. 10, s. 943-51. https://doi.org/10.1593/neo.121092

APA

Lecomte, J., Masset, A., Blacher, S., Maertens, L., Gothot, A., Delgaudine, M., ... Noel, A. (2012). Bone marrow-derived myofibroblasts are the providers of pro-invasive matrix metalloproteinase 13 in primary tumor. Neoplasia, 14(10), 943-51. https://doi.org/10.1593/neo.121092

CBE

Lecomte J, Masset A, Blacher S, Maertens L, Gothot A, Delgaudine M, Bruyère F, Carnet O, Paupert J, Illemann M, Foidart J-M, Lund IK, Høyer-Hansen G, Noel A. 2012. Bone marrow-derived myofibroblasts are the providers of pro-invasive matrix metalloproteinase 13 in primary tumor. Neoplasia. 14(10):943-51. https://doi.org/10.1593/neo.121092

MLA

Vancouver

Author

Lecomte, Julie ; Masset, Anne ; Blacher, Silvia ; Maertens, Ludovic ; Gothot, André ; Delgaudine, Marie ; Bruyère, Françoise ; Carnet, Oriane ; Paupert, Jenny ; Illemann, Martin ; Foidart, Jean-Michel ; Lund, Ida K ; Høyer-Hansen, Gunilla ; Noel, Agnes. / Bone marrow-derived myofibroblasts are the providers of pro-invasive matrix metalloproteinase 13 in primary tumor. I: Neoplasia. 2012 ; Bind 14, Nr. 10. s. 943-51.

Bibtex

@article{19a002d6d2ae4b8abad2a455e8dd54d0,
title = "Bone marrow-derived myofibroblasts are the providers of pro-invasive matrix metalloproteinase 13 in primary tumor",
abstract = "Carcinoma-associated fibroblasts are key contributors of the tumor microenvironment that regulates carcinoma progression. They consist of a heterogeneous cell population with diverse origins, phenotypes, and functions. In the present report, we have explored the contribution of bone marrow (BM)-derived cells to generate different fibroblast subsets that putatively produce the matrix metalloproteinase 13 (MMP13) and affect cancer cell invasion. A murine model of skin carcinoma was applied to mice, irradiated, and engrafted with BM isolated from green fluorescent protein (GFP) transgenic mice. We provide evidence that one third of BM-derived GFP(+) cells infiltrating the tumor expressed the chondroitin sulfate proteoglycan NG2 (pericytic marker) or α-smooth muscle actin (α-SMA, myofibroblast marker), whereas almost 90{\%} of Thy1(+) fibroblasts were originating from resident GFP-negative cells. MMP13producing cells were exclusively α-SMA(+) cells and derived from GFP(+) BM cells. To investigate their impact on tumor invasion, we isolated mesenchymal stem cells (MSCs) from the BM of wild-type and MMP13-deficient mice. Wild-type MSC promoted cancer cell invasion in a spheroid assay, whereas MSCs obtained from MMP13-deficient mice failed to. Our data support the concept of fibroblast subset specialization with BM-derived α-SMA(+) cells being the main source of MMP13, a stromal mediator of cancer cell invasion.",
author = "Julie Lecomte and Anne Masset and Silvia Blacher and Ludovic Maertens and Andr{\'e} Gothot and Marie Delgaudine and Fran{\cc}oise Bruy{\`e}re and Oriane Carnet and Jenny Paupert and Martin Illemann and Jean-Michel Foidart and Lund, {Ida K} and Gunilla H{\o}yer-Hansen and Agnes Noel",
year = "2012",
doi = "10.1593/neo.121092",
language = "English",
volume = "14",
pages = "943--51",
journal = "Neoplasia",
issn = "1522-8002",
publisher = "Neoplasia Press",
number = "10",

}

RIS

TY - JOUR

T1 - Bone marrow-derived myofibroblasts are the providers of pro-invasive matrix metalloproteinase 13 in primary tumor

AU - Lecomte, Julie

AU - Masset, Anne

AU - Blacher, Silvia

AU - Maertens, Ludovic

AU - Gothot, André

AU - Delgaudine, Marie

AU - Bruyère, Françoise

AU - Carnet, Oriane

AU - Paupert, Jenny

AU - Illemann, Martin

AU - Foidart, Jean-Michel

AU - Lund, Ida K

AU - Høyer-Hansen, Gunilla

AU - Noel, Agnes

PY - 2012

Y1 - 2012

N2 - Carcinoma-associated fibroblasts are key contributors of the tumor microenvironment that regulates carcinoma progression. They consist of a heterogeneous cell population with diverse origins, phenotypes, and functions. In the present report, we have explored the contribution of bone marrow (BM)-derived cells to generate different fibroblast subsets that putatively produce the matrix metalloproteinase 13 (MMP13) and affect cancer cell invasion. A murine model of skin carcinoma was applied to mice, irradiated, and engrafted with BM isolated from green fluorescent protein (GFP) transgenic mice. We provide evidence that one third of BM-derived GFP(+) cells infiltrating the tumor expressed the chondroitin sulfate proteoglycan NG2 (pericytic marker) or α-smooth muscle actin (α-SMA, myofibroblast marker), whereas almost 90% of Thy1(+) fibroblasts were originating from resident GFP-negative cells. MMP13producing cells were exclusively α-SMA(+) cells and derived from GFP(+) BM cells. To investigate their impact on tumor invasion, we isolated mesenchymal stem cells (MSCs) from the BM of wild-type and MMP13-deficient mice. Wild-type MSC promoted cancer cell invasion in a spheroid assay, whereas MSCs obtained from MMP13-deficient mice failed to. Our data support the concept of fibroblast subset specialization with BM-derived α-SMA(+) cells being the main source of MMP13, a stromal mediator of cancer cell invasion.

AB - Carcinoma-associated fibroblasts are key contributors of the tumor microenvironment that regulates carcinoma progression. They consist of a heterogeneous cell population with diverse origins, phenotypes, and functions. In the present report, we have explored the contribution of bone marrow (BM)-derived cells to generate different fibroblast subsets that putatively produce the matrix metalloproteinase 13 (MMP13) and affect cancer cell invasion. A murine model of skin carcinoma was applied to mice, irradiated, and engrafted with BM isolated from green fluorescent protein (GFP) transgenic mice. We provide evidence that one third of BM-derived GFP(+) cells infiltrating the tumor expressed the chondroitin sulfate proteoglycan NG2 (pericytic marker) or α-smooth muscle actin (α-SMA, myofibroblast marker), whereas almost 90% of Thy1(+) fibroblasts were originating from resident GFP-negative cells. MMP13producing cells were exclusively α-SMA(+) cells and derived from GFP(+) BM cells. To investigate their impact on tumor invasion, we isolated mesenchymal stem cells (MSCs) from the BM of wild-type and MMP13-deficient mice. Wild-type MSC promoted cancer cell invasion in a spheroid assay, whereas MSCs obtained from MMP13-deficient mice failed to. Our data support the concept of fibroblast subset specialization with BM-derived α-SMA(+) cells being the main source of MMP13, a stromal mediator of cancer cell invasion.

U2 - 10.1593/neo.121092

DO - 10.1593/neo.121092

M3 - Journal article

VL - 14

SP - 943

EP - 951

JO - Neoplasia

JF - Neoplasia

SN - 1522-8002

IS - 10

ER -

ID: 36840014