Loss of p53 triggers WNT-dependent systemic inflammation to drive breast cancer metastasis

Cancer-associated systemic inflammation is strongly linked to poor disease outcome in patients with cancer 1 , 2 . For most human epithelial tumour types, high systemic neutrophil-to-lymphocyte ratios are associated with poor overall survival 3 , and experimental studies have demonstrated a causal r...

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Vydáno v:Nature (London) Ročník 572; číslo 7770; s. 538 - 542
Hlavní autoři: Wellenstein, Max D., Coffelt, Seth B., Duits, Danique E. M., van Miltenburg, Martine H., Slagter, Maarten, de Rink, Iris, Henneman, Linda, Kas, Sjors M., Prekovic, Stefan, Hau, Cheei-Sing, Vrijland, Kim, Drenth, Anne Paulien, de Korte-Grimmerink, Renske, Schut, Eva, van der Heijden, Ingrid, Zwart, Wilbert, Wessels, Lodewyk F. A., Schumacher, Ton N., Jonkers, Jos, de Visser, Karin E.
Médium: Journal Article
Jazyk:angličtina
Vydáno: London Nature Publishing Group UK 01.08.2019
Nature Publishing Group
Témata:
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Analysis
Animal models
Animals
Bioinformatics
Bone marrow
Breast cancer
Breast Neoplasms - complications
Breast Neoplasms - genetics
Breast Neoplasms - pathology
Causes of
CRISPR
Diagnosis
Disease Models, Animal
Female
Gene expression
Genetic aspects
Genetic engineering
Genomes
Heterogeneity
Humanities and Social Sciences
IL-1β
Inflammation
Inflammation - complications
Inflammation - genetics
Inflammation - immunology
Inflammation - pathology
Influence
Interleukin-1beta - immunology
Interleukin-1beta - metabolism
Letter
Leukocytes (neutrophilic)
Ligands
Lymphocytes
Macrophages
Metastases
Metastasis
Mice
multidisciplinary
Mutation
Neoplasm Metastasis - pathology
Neutrophilia
Neutrophils
Neutrophils - immunology
p53 Protein
Principal components analysis
Science
Science (multidisciplinary)
Tumor proteins
Tumor Suppressor Protein p53 - deficiency
Tumor Suppressor Protein p53 - genetics
Tumors
Wnt protein
Wnt proteins
Wnt Proteins - metabolism
Netherlands
ISSN:0028-0836, 1476-4687, 1476-4687
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Abstract Cancer-associated systemic inflammation is strongly linked to poor disease outcome in patients with cancer 1 , 2 . For most human epithelial tumour types, high systemic neutrophil-to-lymphocyte ratios are associated with poor overall survival 3 , and experimental studies have demonstrated a causal relationship between neutrophils and metastasis 4 , 5 . However, the cancer-cell-intrinsic mechanisms that dictate the substantial heterogeneity in systemic neutrophilic inflammation between tumour-bearing hosts are largely unresolved. Here, using a panel of 16 distinct genetically engineered mouse models for breast cancer, we uncover a role for cancer-cell-intrinsic p53 as a key regulator of pro-metastatic neutrophils. Mechanistically, loss of p53 in cancer cells induced the secretion of WNT ligands that stimulate tumour-associated macrophages to produce IL-1β, thus driving systemic inflammation. Pharmacological and genetic blockade of WNT secretion in p53-null cancer cells reverses macrophage production of IL-1β and subsequent neutrophilic inflammation, resulting in reduced metastasis formation. Collectively, we demonstrate a mechanistic link between the loss of p53 in cancer cells, secretion of WNT ligands and systemic neutrophilia that potentiates metastatic progression. These insights illustrate the importance of the genetic makeup of breast tumours in dictating pro-metastatic systemic inflammation, and set the stage for personalized immune intervention strategies for patients with cancer. Loss of p53 in mouse models of breast cancer leads to activation of WNT signalling, which promotes metastatic spread by inducing systemic neutrophilic inflammation.
AbstractList Cancer-associated systemic inflammation is strongly linked to poor disease outcome in patients with cancer.sup.1,2. For most human epithelial tumour types, high systemic neutrophil-to-lymphocyte ratios are associated with poor overall survival.sup.3, and experimental studies have demonstrated a causal relationship between neutrophils and metastasis.sup.4,5. However, the cancer-cell-intrinsic mechanisms that dictate the substantial heterogeneity in systemic neutrophilic inflammation between tumour-bearing hosts are largely unresolved. Here, using a panel of 16 distinct genetically engineered mouse models for breast cancer, we uncover a role for cancer-cell-intrinsic p53 as a key regulator of pro-metastatic neutrophils. Mechanistically, loss of p53 in cancer cells induced the secretion of WNT ligands that stimulate tumour-associated macrophages to produce IL-1[beta], thus driving systemic inflammation. Pharmacological and genetic blockade of WNT secretion in p53-null cancer cells reverses macrophage production of IL-1[beta] and subsequent neutrophilic inflammation, resulting in reduced metastasis formation. Collectively, we demonstrate a mechanistic link between the loss of p53 in cancer cells, secretion of WNT ligands and systemic neutrophilia that potentiates metastatic progression. These insights illustrate the importance of the genetic makeup of breast tumours in dictating pro-metastatic systemic inflammation, and set the stage for personalized immune intervention strategies for patients with cancer. Loss of p53 in mouse models of breast cancer leads to activation of WNT signalling, which promotes metastatic spread by inducing systemic neutrophilic inflammation.
Cancer-associated systemic inflammation is strongly linked to poor disease outcome in patients with cancer.sup.1,2. For most human epithelial tumour types, high systemic neutrophil-to-lymphocyte ratios are associated with poor overall survival.sup.3, and experimental studies have demonstrated a causal relationship between neutrophils and metastasis.sup.4,5. However, the cancer-cell-intrinsic mechanisms that dictate the substantial heterogeneity in systemic neutrophilic inflammation between tumour-bearing hosts are largely unresolved. Here, using a panel of 16 distinct genetically engineered mouse models for breast cancer, we uncover a role for cancer-cell-intrinsic p53 as a key regulator of pro-metastatic neutrophils. Mechanistically, loss of p53 in cancer cells induced the secretion of WNT ligands that stimulate tumour-associated macrophages to produce IL-1[beta], thus driving systemic inflammation. Pharmacological and genetic blockade of WNT secretion in p53-null cancer cells reverses macrophage production of IL-1[beta] and subsequent neutrophilic inflammation, resulting in reduced metastasis formation. Collectively, we demonstrate a mechanistic link between the loss of p53 in cancer cells, secretion of WNT ligands and systemic neutrophilia that potentiates metastatic progression. These insights illustrate the importance of the genetic makeup of breast tumours in dictating pro-metastatic systemic inflammation, and set the stage for personalized immune intervention strategies for patients with cancer.
Cancer-associated systemic inflammation is strongly linked to poor disease outcome in patients with cancer1,2. For most human epithelial tumour types, high systemic neutrophil-to-lymphocyte ratios are associated with poor overall survival3, and experimental studies have demonstrated a causal relationship between neutrophils and metastasis4,5. However, the cancer-cell-intrinsic mechanisms that dictate the substantial heterogeneity in systemic neutrophilic inflammation between tumour-bearing hosts are largely unresolved. Here, using a panel of 16 distinct genetically engineered mouse models for breast cancer, we uncover a role for cancer-cell-intrinsic p53 as a key regulator of pro-metastatic neutrophils. Mechanistically, loss of p53 in cancer cells induced the secretion of WNT ligands that stimulate tumour-associated macrophages to produce IL-1β, thus driving systemic inflammation. Pharmacological and genetic blockade of WNT secretion in p53-null cancer cells reverses macrophage production of IL-1β and subsequent neutrophilic inflammation, resulting in reduced metastasis formation. Collectively, we demonstrate a mechanistic link between the loss of p53 in cancer cells, secretion of WNT ligands and systemic neutrophilia that potentiates metastatic progression. These insights illustrate the importance of the genetic makeup of breast tumours in dictating pro-metastatic systemic inflammation, and set the stage for personalized immune intervention strategies for patients with cancer.Cancer-associated systemic inflammation is strongly linked to poor disease outcome in patients with cancer1,2. For most human epithelial tumour types, high systemic neutrophil-to-lymphocyte ratios are associated with poor overall survival3, and experimental studies have demonstrated a causal relationship between neutrophils and metastasis4,5. However, the cancer-cell-intrinsic mechanisms that dictate the substantial heterogeneity in systemic neutrophilic inflammation between tumour-bearing hosts are largely unresolved. Here, using a panel of 16 distinct genetically engineered mouse models for breast cancer, we uncover a role for cancer-cell-intrinsic p53 as a key regulator of pro-metastatic neutrophils. Mechanistically, loss of p53 in cancer cells induced the secretion of WNT ligands that stimulate tumour-associated macrophages to produce IL-1β, thus driving systemic inflammation. Pharmacological and genetic blockade of WNT secretion in p53-null cancer cells reverses macrophage production of IL-1β and subsequent neutrophilic inflammation, resulting in reduced metastasis formation. Collectively, we demonstrate a mechanistic link between the loss of p53 in cancer cells, secretion of WNT ligands and systemic neutrophilia that potentiates metastatic progression. These insights illustrate the importance of the genetic makeup of breast tumours in dictating pro-metastatic systemic inflammation, and set the stage for personalized immune intervention strategies for patients with cancer.
Cancer-associated systemic inflammation is strongly linked to poor disease outcome in patients with cancer 1 , 2 . For most human epithelial tumour types, high systemic neutrophil-to-lymphocyte ratios are associated with poor overall survival 3 , and experimental studies have demonstrated a causal relationship between neutrophils and metastasis 4 , 5 . However, the cancer-cell-intrinsic mechanisms that dictate the substantial heterogeneity in systemic neutrophilic inflammation between tumour-bearing hosts are largely unresolved. Here, using a panel of 16 distinct genetically engineered mouse models for breast cancer, we uncover a role for cancer-cell-intrinsic p53 as a key regulator of pro-metastatic neutrophils. Mechanistically, loss of p53 in cancer cells induced the secretion of WNT ligands that stimulate tumour-associated macrophages to produce IL-1β, thus driving systemic inflammation. Pharmacological and genetic blockade of WNT secretion in p53-null cancer cells reverses macrophage production of IL-1β and subsequent neutrophilic inflammation, resulting in reduced metastasis formation. Collectively, we demonstrate a mechanistic link between the loss of p53 in cancer cells, secretion of WNT ligands and systemic neutrophilia that potentiates metastatic progression. These insights illustrate the importance of the genetic makeup of breast tumours in dictating pro-metastatic systemic inflammation, and set the stage for personalized immune intervention strategies for patients with cancer. Loss of p53 in mouse models of breast cancer leads to activation of WNT signalling, which promotes metastatic spread by inducing systemic neutrophilic inflammation.
Cancer-associated systemic inflammation is strongly linked with poor disease outcome in cancer patients1,2. For most human epithelial tumour types, high systemic neutrophil-to-lymphocyte ratios are associated with poor overall survival3, and experimental studies have demonstrated a causal relationship between neutrophils and metastasis4,5. However, the cancer cell-intrinsic mechanisms dictating the substantial heterogeneity in systemic neutrophilic inflammation between tumour-bearing hosts are largely unresolved. Using a panel of 16 distinct genetically engineered mouse models (GEMMs) for breast cancer, we have uncovered a novel role for cancer cell-intrinsic p53 as a key regulator of pro-metastatic neutrophils. Mechanistically, p53 loss in cancer cells induced secretion of Wnt ligands that stimulate IL-1β production by tumour-associated macrophages, which drives systemic inflammation. Pharmacological and genetic blockade of Wnt secretion in p53-null cancer cells reverses IL-1β expression by macrophages and subsequent neutrophilic inflammation, resulting in reduced metastasis formation. Collectively, we demonstrate a novel mechanistic link between loss of p53 in cancer cells, Wnt ligand secretion and systemic neutrophilia that potentiates metastatic progression. These insights illustrate the importance of the genetic makeup of breast tumours in dictating pro-metastatic systemic inflammation, and set the stage for personalized immune intervention strategies for cancer patients.
Cancer-associated systemic inflammation is strongly linked to poor disease outcome in patients with cancer. For most human epithelial tumour types, high systemic neutrophil-to-lymphocyte ratios are associated with poor overall survival, and experimental studies have demonstrated a causal relationship between neutrophils and metastasis. However, the cancer-cell-intrinsic mechanisms that dictate the substantial heterogeneity in systemic neutrophilic inflammation between tumour-bearing hosts are largely unresolved. Here, using a panel of 16 distinct genetically engineered mouse models for breast cancer, we uncover a role for cancer-cell-intrinsic p53 as a key regulator of pro-metastatic neutrophils. Mechanistically, loss of p53 in cancer cells induced the secretion of WNT ligands that stimulate tumour-associated macrophages to produce IL-1β, thus driving systemic inflammation. Pharmacological and genetic blockade of WNT secretion in p53-null cancer cells reverses macrophage production of IL-1β and subsequent neutrophilic inflammation, resulting in reduced metastasis formation. Collectively, we demonstrate a mechanistic link between the loss of p53 in cancer cells, secretion of WNT ligands and systemic neutrophilia that potentiates metastatic progression. These insights illustrate the importance of the genetic makeup of breast tumours in dictating pro-metastatic systemic inflammation, and set the stage for personalized immune intervention strategies for patients with cancer.
Cancer-associated systemic inflammation is strongly linked to poor disease outcome in patients with cancer . For most human epithelial tumour types, high systemic neutrophil-to-lymphocyte ratios are associated with poor overall survival , and experimental studies have demonstrated a causal relationship between neutrophils and metastasis . However, the cancer-cell-intrinsic mechanisms that dictate the substantial heterogeneity in systemic neutrophilic inflammation between tumour-bearing hosts are largely unresolved. Here, using a panel of 16 distinct genetically engineered mouse models for breast cancer, we uncover a role for cancer-cell-intrinsic p53 as a key regulator of pro-metastatic neutrophils. Mechanistically, loss of p53 in cancer cells induced the secretion of WNT ligands that stimulate tumour-associated macrophages to produce IL-1β, thus driving systemic inflammation. Pharmacological and genetic blockade of WNT secretion in p53-null cancer cells reverses macrophage production of IL-1β and subsequent neutrophilic inflammation, resulting in reduced metastasis formation. Collectively, we demonstrate a mechanistic link between the loss of p53 in cancer cells, secretion of WNT ligands and systemic neutrophilia that potentiates metastatic progression. These insights illustrate the importance of the genetic makeup of breast tumours in dictating pro-metastatic systemic inflammation, and set the stage for personalized immune intervention strategies for patients with cancer.
Audience Academic
Author Schut, Eva
Coffelt, Seth B.
Duits, Danique E. M.
de Korte-Grimmerink, Renske
Zwart, Wilbert
Slagter, Maarten
Vrijland, Kim
Hau, Cheei-Sing
Prekovic, Stefan
Kas, Sjors M.
Wessels, Lodewyk F. A.
Schumacher, Ton N.
de Rink, Iris
Jonkers, Jos
van Miltenburg, Martine H.
Wellenstein, Max D.
Henneman, Linda
van der Heijden, Ingrid
de Visser, Karin E.
Drenth, Anne Paulien
AuthorAffiliation 3 Division of Molecular Pathology, Oncode Institute, Netherlands Cancer Institute, 1066CX Amsterdam, The Netherlands
4 Division of Molecular Oncology & Immunology, Oncode Institute, Netherlands Cancer Institute, 1066CX Amsterdam, The Netherlands
8 Division of Oncogenomics, Oncode Institute, Netherlands Cancer Institute, 1066CX Amsterdam, The Netherlands
1 Division of Tumour Biology & Immunology, Oncode Institute, Netherlands Cancer Institute, 1066CX Amsterdam, The Netherlands
5 Division of Molecular Carcinogenesis, Oncode Institute, Netherlands Cancer Institute, 1066CX Amsterdam, The Netherlands
6 Genomics Core Facility, Netherlands Cancer Institute, 1066CX Amsterdam, The Netherlands
7 Mouse Clinic for Cancer and Aging, Netherlands Cancer Institute, 1066CX Amsterdam, The Netherlands
AuthorAffiliation_xml – name: 8 Division of Oncogenomics, Oncode Institute, Netherlands Cancer Institute, 1066CX Amsterdam, The Netherlands
– name: 6 Genomics Core Facility, Netherlands Cancer Institute, 1066CX Amsterdam, The Netherlands
– name: 3 Division of Molecular Pathology, Oncode Institute, Netherlands Cancer Institute, 1066CX Amsterdam, The Netherlands
– name: 7 Mouse Clinic for Cancer and Aging, Netherlands Cancer Institute, 1066CX Amsterdam, The Netherlands
– name: 4 Division of Molecular Oncology & Immunology, Oncode Institute, Netherlands Cancer Institute, 1066CX Amsterdam, The Netherlands
– name: 1 Division of Tumour Biology & Immunology, Oncode Institute, Netherlands Cancer Institute, 1066CX Amsterdam, The Netherlands
– name: 5 Division of Molecular Carcinogenesis, Oncode Institute, Netherlands Cancer Institute, 1066CX Amsterdam, The Netherlands
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  organization: Division of Tumour Biology & Immunology, Oncode Institute, Netherlands Cancer Institute, Institute of Cancer Sciences, University of Glasgow, Cancer Research UK Beatson Institute
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  organization: Mouse Clinic for Cancer and Aging, Netherlands Cancer Institute
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  surname: Kas
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/31367040$$D View this record in MEDLINE/PubMed
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Current address: Institute of Cancer Sciences, University of Glasgow and Cancer Research UK Beatson Institute, Glasgow G61 1BD, UK.
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Snippet Cancer-associated systemic inflammation is strongly linked to poor disease outcome in patients with cancer 1 , 2 . For most human epithelial tumour types, high...
Cancer-associated systemic inflammation is strongly linked to poor disease outcome in patients with cancer . For most human epithelial tumour types, high...
Cancer-associated systemic inflammation is strongly linked to poor disease outcome in patients with cancer.sup.1,2. For most human epithelial tumour types,...
Cancer-associated systemic inflammation is strongly linked to poor disease outcome in patients with cancer. For most human epithelial tumour types, high...
Cancer-associated systemic inflammation is strongly linked to poor disease outcome in patients with cancer1,2. For most human epithelial tumour types, high...
Cancer-associated systemic inflammation is strongly linked with poor disease outcome in cancer patients1,2. For most human epithelial tumour types, high...
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Analysis
Animal models
Animals
Bioinformatics
Bone marrow
Breast cancer
Breast Neoplasms - complications
Breast Neoplasms - genetics
Breast Neoplasms - pathology
Causes of
CRISPR
Diagnosis
Disease Models, Animal
Female
Gene expression
Genetic aspects
Genetic engineering
Genomes
Heterogeneity
Humanities and Social Sciences
IL-1β
Inflammation
Inflammation - complications
Inflammation - genetics
Inflammation - immunology
Inflammation - pathology
Influence
Interleukin-1beta - immunology
Interleukin-1beta - metabolism
Letter
Leukocytes (neutrophilic)
Ligands
Lymphocytes
Macrophages
Metastases
Metastasis
Mice
multidisciplinary
Mutation
Neoplasm Metastasis - pathology
Neutrophilia
Neutrophils
Neutrophils - immunology
p53 Protein
Principal components analysis
Science
Science (multidisciplinary)
Tumor proteins
Tumor Suppressor Protein p53 - deficiency
Tumor Suppressor Protein p53 - genetics
Tumors
Wnt protein
Wnt proteins
Wnt Proteins - metabolism
Title Loss of p53 triggers WNT-dependent systemic inflammation to drive breast cancer metastasis
URI https://link.springer.com/article/10.1038/s41586-019-1450-6
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Volume 572
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