Macrophage-derived SPARC bridges tumor cell-extracellular matrix interactions toward metastasis

Sabina Sangaletti; Emma Di Carlo; Silvia Gariboldi; Silvia Miotti; Barbara Cappetti; Mariella Parenza; Cristiano Rumio; Rolf A. Brekken; Claudia Chiodoni; Mario P. Colombo

doi:10.1158/0008-5472.CAN-08-1327

Macrophage-derived SPARC bridges tumor cell-extracellular matrix interactions toward metastasis

Sabina Sangaletti, Emma Di Carlo, Silvia Gariboldi, Silvia Miotti, Barbara Cappetti, Mariella Parenza, Cristiano Rumio, Rolf A. Brekken, Claudia Chiodoni, Mario P. Colombo

Research output: Contribution to journal › Article › peer-review

164 Scopus citations

Abstract

Other than genetic imprinting and epithelial to mesenchymal transition, cancer cells need interaction with the nearby stroma toward metastasis. Secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein known to regulate extracellular matrix (ECM) deposition and cell-ECM interaction. Gene expression profiles associate SPARC to malignant progression. Using reciprocal bone marrow chimeras between SPARC knockout and wild-type mice, we show that SPARC produced by inflammatory cells is necessary for spontaneous, but not experimental, i.v. metastasis. Macrophage-derived SPARC induces cancer cell migration and enhances their migration to other ECM proteins at least through α_vβ₅ integrin. Indeed, RNA interference knockdown of β₅ integrin expression reduces cell migration in vitro and metastasis in vivo. Together these results show that macrophage-derived SPARC takes part in metastasis, acting at the step of integrin-mediated migration of invasive cells.

Original language	English (US)
Pages (from-to)	9050-9059
Number of pages	10
Journal	Cancer research
Volume	68
Issue number	21
DOIs	https://doi.org/10.1158/0008-5472.CAN-08-1327
State	Published - Nov 1 2008

ASJC Scopus subject areas

Oncology
Cancer Research

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10.1158/0008-5472.CAN-08-1327

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title = "Macrophage-derived SPARC bridges tumor cell-extracellular matrix interactions toward metastasis",

abstract = "Other than genetic imprinting and epithelial to mesenchymal transition, cancer cells need interaction with the nearby stroma toward metastasis. Secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein known to regulate extracellular matrix (ECM) deposition and cell-ECM interaction. Gene expression profiles associate SPARC to malignant progression. Using reciprocal bone marrow chimeras between SPARC knockout and wild-type mice, we show that SPARC produced by inflammatory cells is necessary for spontaneous, but not experimental, i.v. metastasis. Macrophage-derived SPARC induces cancer cell migration and enhances their migration to other ECM proteins at least through αvβ5 integrin. Indeed, RNA interference knockdown of β5 integrin expression reduces cell migration in vitro and metastasis in vivo. Together these results show that macrophage-derived SPARC takes part in metastasis, acting at the step of integrin-mediated migration of invasive cells.",

author = "Sabina Sangaletti and {Di Carlo}, Emma and Silvia Gariboldi and Silvia Miotti and Barbara Cappetti and Mariella Parenza and Cristiano Rumio and Brekken, {Rolf A.} and Claudia Chiodoni and Colombo, {Mario P.}",

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AU - Sangaletti, Sabina

AU - Di Carlo, Emma

AU - Gariboldi, Silvia

AU - Miotti, Silvia

AU - Cappetti, Barbara

AU - Parenza, Mariella

AU - Rumio, Cristiano

AU - Brekken, Rolf A.

AU - Chiodoni, Claudia

AU - Colombo, Mario P.

PY - 2008/11/1

Y1 - 2008/11/1

N2 - Other than genetic imprinting and epithelial to mesenchymal transition, cancer cells need interaction with the nearby stroma toward metastasis. Secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein known to regulate extracellular matrix (ECM) deposition and cell-ECM interaction. Gene expression profiles associate SPARC to malignant progression. Using reciprocal bone marrow chimeras between SPARC knockout and wild-type mice, we show that SPARC produced by inflammatory cells is necessary for spontaneous, but not experimental, i.v. metastasis. Macrophage-derived SPARC induces cancer cell migration and enhances their migration to other ECM proteins at least through αvβ5 integrin. Indeed, RNA interference knockdown of β5 integrin expression reduces cell migration in vitro and metastasis in vivo. Together these results show that macrophage-derived SPARC takes part in metastasis, acting at the step of integrin-mediated migration of invasive cells.

AB - Other than genetic imprinting and epithelial to mesenchymal transition, cancer cells need interaction with the nearby stroma toward metastasis. Secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein known to regulate extracellular matrix (ECM) deposition and cell-ECM interaction. Gene expression profiles associate SPARC to malignant progression. Using reciprocal bone marrow chimeras between SPARC knockout and wild-type mice, we show that SPARC produced by inflammatory cells is necessary for spontaneous, but not experimental, i.v. metastasis. Macrophage-derived SPARC induces cancer cell migration and enhances their migration to other ECM proteins at least through αvβ5 integrin. Indeed, RNA interference knockdown of β5 integrin expression reduces cell migration in vitro and metastasis in vivo. Together these results show that macrophage-derived SPARC takes part in metastasis, acting at the step of integrin-mediated migration of invasive cells.

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JO - Cancer research

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ER -

Macrophage-derived SPARC bridges tumor cell-extracellular matrix interactions toward metastasis

Abstract

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