Matrix remodeling stimulates stromal autophagy, "fueling" cancer cell mitochondrial metabolism and metastasis

We have previously demonstrated that loss of stromal caveolin-1 (Cav-1) in cancer-associated fibroblasts is a strong and independent predictor of poor clinical outcome in human breast cancer patients. However, the signaling mechanism(s) by which Cav-1 downregulation leads to this tumor-promoting mic...

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Veröffentlicht in:	Cell cycle (Georgetown, Tex.) Jg. 10; H. 12; S. 2021 - 2034
Hauptverfasser:	Castello-Cros, Remedios, Bonnuccelli, Gloria, Molchansky, Alex, Capozza, Franco, Witkiewicz, Agnieszka K., Birbe, Ruth, Howell, Anthony, Pestell, Richard G., Whitaker-Menezes, Diana, Sotgia, Federica, Lisanti, Michael P
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	United States Taylor & Francis 15.06.2011 Landes Bioscience
Schlagworte:	Animals Autophagy Binding Biology Bioscience Breast Neoplasms - pathology Calcium Cancer Caveolin 1 - metabolism Cell Cell Line, Tumor Coculture Techniques Cycle Extracellular Matrix - metabolism Fibroblasts - pathology Humans Landes Mice Mitochondria - metabolism Mitochondria - pathology Neoplasm Metastasis Neoplasms - pathology Neoplasms - ultrastructure Organogenesis Plasminogen Activator Inhibitor 1 - metabolism Plasminogen Activator Inhibitor 2 - metabolism Proteins Stromal Cells - pathology Transplantation, Heterologous Tumor Microenvironment
ISSN:	1538-4101, 1551-4005, 1551-4005
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Abstract	We have previously demonstrated that loss of stromal caveolin-1 (Cav-1) in cancer-associated fibroblasts is a strong and independent predictor of poor clinical outcome in human breast cancer patients. However, the signaling mechanism(s) by which Cav-1 downregulation leads to this tumor-promoting microenvironment are not well understood. To address this issue, we performed an unbiased comparative proteomic analysis of wild-type (WT) and Cav-1 -/- null mammary stromal fibroblasts (MSFs). Our results show that plasminogen activator inhibitor type 1 and type 2 (PAI-1 and PAI-2) expression is significantly increased in Cav-1 -/- MSFs. To establish a direct cause-effect relationship, we next generated immortalized human fibroblast lines stably overexpressing either PAI-1 or PAI-2. Importantly, PAI-1/2(+) fibroblasts promote the growth of MDA-MB-231 tumors (a human breast cancer cell line) in a murine xenograft model, without any increases in angiogenesis. Similarly, PAI-1/2(+) fibroblasts stimulate experimental metastasis of MDA-MB-231 cells using an in vivo lung colonization assay. Further mechanistic studies revealed that fibroblasts overexpressing PAI-1 or PAI-2 display increased autophagy ("self-eating") and are sufficient to induce mitochondrial biogenesis/activity in adjacent cancer cells, in co-culture experiments. In xenografts, PAI-1/2(+) fibroblasts significantly reduce the apoptosis of MDA-MB-231 tumor cells. The current study provides further support for the "Autophagic Tumor Stroma Model of Cancer" and identifies a novel "extracellular matrix"-based signaling mechanism, by which a loss of stromal Cav-1 generates a metastatic phenotype. Thus, the secretion and remodeling of extracellular matrix components (such as PAI-1/2) can directly regulate both (1) autophagy in stromal fibroblasts and (2) epithelial tumor cell mitochondrial metabolism.
AbstractList	We have previously demonstrated that loss of stromal caveolin-1 (Cav-1) in cancer-associated fibroblasts is a strong and independent predictor of poor clinical outcome in human breast cancer patients. However, the signaling mechanism(s) by which Cav-1 downregulation leads to this tumor-promoting microenvironment are not well understood. To address this issue, we performed an unbiased comparative proteomic analysis of wild-type (WT) and Cav-1 -/- null mammary stromal fibroblasts (MSFs). Our results show that plasminogen activator inhibitor type 1 and type 2 (PAI-1 and PAI-2) expression is significantly increased in Cav-1 -/- MSFs. To establish a direct cause-effect relationship, we next generated immortalized human fibroblast lines stably overexpressing either PAI-1 or PAI-2. Importantly, PAI-1/2(+) fibroblasts promote the growth of MDA-MB-231 tumors (a human breast cancer cell line) in a murine xenograft model, without any increases in angiogenesis. Similarly, PAI-1/2(+) fibroblasts stimulate experimental metastasis of MDA-MB-231 cells using an in vivo lung colonization assay. Further mechanistic studies revealed that fibroblasts overexpressing PAI-1 or PAI-2 display increased autophagy ("self-eating") and are sufficient to induce mitochondrial biogenesis/activity in adjacent cancer cells, in co-culture experiments. In xenografts, PAI-1/2(+) fibroblasts significantly reduce the apoptosis of MDA-MB-231 tumor cells. The current study provides further support for the "Autophagic Tumor Stroma Model of Cancer" and identifies a novel "extracellular matrix"-based signaling mechanism, by which a loss of stromal Cav-1 generates a metastatic phenotype. Thus, the secretion and remodeling of extracellular matrix components (such as PAI-1/2) can directly regulate both (1) autophagy in stromal fibroblasts and (2) epithelial tumor cell mitochondrial metabolism. We have previously demonstrated that loss of stromal caveolin-1 (Cav-1) in cancer-associated fibroblasts is a strong and independent predictor of poor clinical outcome in human breast cancer patients. However, the signaling mechanism(s) by which Cav-1 downregulation leads to this tumor-promoting microenvironment are not well understood. To address this issue, we performed an unbiased comparative proteomic analysis of wild-type (WT) and Cav-1-/- null mammary stromal fibroblasts (MSFs). Our results show that plasminogen activator inhibitor type 1 and type 2 (PAI-1 and PAI-2) expression is significantly increased in Cav-1-/- MSFs. To establish a direct cause-effect relationship, we next generated immortalized human fibroblast lines stably overexpressing either PAI-1 or PAI-2. Importantly, PAI-1/2(+) fibroblasts promote the growth of MDA-MB-231 tumors (a human breast cancer cell line) in a murine xenograft model, without any increases in angiogenesis. Similarly, PAI-1/2(+) fibroblasts stimulate experimental metastasis of MDA-MB-231 cells using an in vivo lung colonization assay. Further mechanistic studies revealed that fibroblasts overexpressing PAI-1 or PAI-2 display increased autophagy (“self-eating”) and are sufficient to induce mitochondrial biogenesis/activity in adjacent cancer cells, in co-culture experiments. In xenografts, PAI-1/2(+) fibroblasts significantly reduce the apoptosis of MDA-MB-231 tumor cells. The current study provides further support for the “Autophagic Tumor Stroma Model of Cancer” and identifies a novel “extracellular matrix”-based signaling mechanism, by which a loss of stromal Cav-1 generates a metastatic phenotype. Thus, the secretion and remodeling of extracellular matrix components (such as PAI-1/2) can directly regulate both (1) autophagy in stromal fibroblasts and (2) epithelial tumor cell mitochondrial metabolism. We have previously demonstrated that loss of stromal caveolin-1 (Cav-1) in cancer-associated fibroblasts is a strong and independent predictor of poor clinical outcome in human breast cancer patients. However, the signaling mechanism(s) by which Cav-1 downregulation leads to this tumor-promoting microenvironment are not well understood. To address this issue, we performed an unbiased comparative proteomic analysis of wild-type (WT) and Cav-1(-/-) null mammary stromal fibroblasts (MSFs). Our results show that plasminogen activator inhibitor type 1 and type 2 (PAI-1 and PAI-2) expression is significantly increased in Cav-1(-/-) MSFs. To establish a direct cause-effect relationship, we next generated immortalized human fibroblast lines stably overexpressing either PAI-1 or PAI-2. Importantly, PAI-1/2(+) fibroblasts promote the growth of MDA-MB-231 tumors (a human breast cancer cell line) in a murine xenograft model, without any increases in angiogenesis. Similarly, PAI-1/2(+) fibroblasts stimulate experimental metastasis of MDA-MB-231 cells using an in vivo lung colonization assay. Further mechanistic studies revealed that fibroblasts overexpressing PAI-1 or PAI-2 display increased autophagy ("self-eating") and are sufficient to induce mitochondrial biogenesis/activity in adjacent cancer cells, in co-culture experiments. In xenografts, PAI-1/2(+) fibroblasts significantly reduce the apoptosis of MDA-MB-231 tumor cells. The current study provides further support for the "Autophagic Tumor Stroma Model of Cancer" and identifies a novel "extracellular matrix"-based signaling mechanism, by which a loss of stromal Cav-1 generates a metastatic phenotype. Thus, the secretion and remodeling of extracellular matrix components (such as PAI-1/2) can directly regulate both (1) autophagy in stromal fibroblasts and (2) epithelial tumor cell mitochondrial metabolism.We have previously demonstrated that loss of stromal caveolin-1 (Cav-1) in cancer-associated fibroblasts is a strong and independent predictor of poor clinical outcome in human breast cancer patients. However, the signaling mechanism(s) by which Cav-1 downregulation leads to this tumor-promoting microenvironment are not well understood. To address this issue, we performed an unbiased comparative proteomic analysis of wild-type (WT) and Cav-1(-/-) null mammary stromal fibroblasts (MSFs). Our results show that plasminogen activator inhibitor type 1 and type 2 (PAI-1 and PAI-2) expression is significantly increased in Cav-1(-/-) MSFs. To establish a direct cause-effect relationship, we next generated immortalized human fibroblast lines stably overexpressing either PAI-1 or PAI-2. Importantly, PAI-1/2(+) fibroblasts promote the growth of MDA-MB-231 tumors (a human breast cancer cell line) in a murine xenograft model, without any increases in angiogenesis. Similarly, PAI-1/2(+) fibroblasts stimulate experimental metastasis of MDA-MB-231 cells using an in vivo lung colonization assay. Further mechanistic studies revealed that fibroblasts overexpressing PAI-1 or PAI-2 display increased autophagy ("self-eating") and are sufficient to induce mitochondrial biogenesis/activity in adjacent cancer cells, in co-culture experiments. In xenografts, PAI-1/2(+) fibroblasts significantly reduce the apoptosis of MDA-MB-231 tumor cells. The current study provides further support for the "Autophagic Tumor Stroma Model of Cancer" and identifies a novel "extracellular matrix"-based signaling mechanism, by which a loss of stromal Cav-1 generates a metastatic phenotype. Thus, the secretion and remodeling of extracellular matrix components (such as PAI-1/2) can directly regulate both (1) autophagy in stromal fibroblasts and (2) epithelial tumor cell mitochondrial metabolism.
Author	Capozza, Franco Molchansky, Alex Whitaker-Menezes, Diana Witkiewicz, Agnieszka K. Castello-Cros, Remedios Sotgia, Federica Bonnuccelli, Gloria Pestell, Richard G. Lisanti, Michael P Howell, Anthony Birbe, Ruth
AuthorAffiliation	4 Manchester Breast Centre and Breakthrough Breast Cancer Research Unit; Paterson Institute for Cancer Research; School of Cancer; Enabling Sciences and Technology; Manchester Academic Health Science Centre; University of Manchester; Machester UK 5 Department of Medical Oncology; Kimmel Cancer Center; Thomas Jefferson University; Philadelphia, PA USA 3 Department of Pathology, Anatomy and Cell Biology; Kimmel Cancer Center; Thomas Jefferson University; Philadelphia, PA USA 1 The Jefferson Stem Cell Biology and Regenerative Medicine Center; Thomas Jefferson University; Philadelphia, PA USA 2 Departments of Stem Cell Biology and Regenerative Medicine and Cancer Biology; Kimmel Cancer Center; Thomas Jefferson University; Philadelphia, PA USA
AuthorAffiliation_xml	– name: 2 Departments of Stem Cell Biology and Regenerative Medicine and Cancer Biology; Kimmel Cancer Center; Thomas Jefferson University; Philadelphia, PA USA – name: 3 Department of Pathology, Anatomy and Cell Biology; Kimmel Cancer Center; Thomas Jefferson University; Philadelphia, PA USA – name: 1 The Jefferson Stem Cell Biology and Regenerative Medicine Center; Thomas Jefferson University; Philadelphia, PA USA – name: 5 Department of Medical Oncology; Kimmel Cancer Center; Thomas Jefferson University; Philadelphia, PA USA – name: 4 Manchester Breast Centre and Breakthrough Breast Cancer Research Unit; Paterson Institute for Cancer Research; School of Cancer; Enabling Sciences and Technology; Manchester Academic Health Science Centre; University of Manchester; Machester UK
Author_xml	– sequence: 1 givenname: Remedios surname: Castello-Cros fullname: Castello-Cros, Remedios email: remedios.castello@jefferson.edu, michaelp.lisanti@gmail.com – sequence: 2 givenname: Gloria surname: Bonnuccelli fullname: Bonnuccelli, Gloria – sequence: 3 givenname: Alex surname: Molchansky fullname: Molchansky, Alex – sequence: 4 givenname: Franco surname: Capozza fullname: Capozza, Franco – sequence: 5 givenname: Agnieszka K. surname: Witkiewicz fullname: Witkiewicz, Agnieszka K. – sequence: 6 givenname: Ruth surname: Birbe fullname: Birbe, Ruth – sequence: 7 givenname: Anthony surname: Howell fullname: Howell, Anthony – sequence: 8 givenname: Richard G. surname: Pestell fullname: Pestell, Richard G. – sequence: 9 givenname: Diana surname: Whitaker-Menezes fullname: Whitaker-Menezes, Diana – sequence: 10 givenname: Federica surname: Sotgia fullname: Sotgia, Federica – sequence: 11 givenname: Michael P surname: Lisanti fullname: Lisanti, Michael P email: remedios.castello@jefferson.edu, michaelp.lisanti@gmail.com
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/21646868$$D View this record in MEDLINE/PubMed
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Snippet	We have previously demonstrated that loss of stromal caveolin-1 (Cav-1) in cancer-associated fibroblasts is a strong and independent predictor of poor clinical...
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SubjectTerms	Animals Autophagy Binding Biology Bioscience Breast Neoplasms - pathology Calcium Cancer Caveolin 1 - metabolism Cell Cell Line, Tumor Coculture Techniques Cycle Extracellular Matrix - metabolism Fibroblasts - pathology Humans Landes Mice Mitochondria - metabolism Mitochondria - pathology Neoplasm Metastasis Neoplasms - pathology Neoplasms - ultrastructure Organogenesis Plasminogen Activator Inhibitor 1 - metabolism Plasminogen Activator Inhibitor 2 - metabolism Proteins Stromal Cells - pathology Transplantation, Heterologous Tumor Microenvironment
Title	Matrix remodeling stimulates stromal autophagy, "fueling" cancer cell mitochondrial metabolism and metastasis
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