Stromal cell diversity associated with immune evasion in human triple‐negative breast cancer

The tumour stroma regulates nearly all stages of carcinogenesis. Stromal heterogeneity in human triple‐negative breast cancers (TNBCs) remains poorly understood, limiting the development of stromal‐targeted therapies. Single‐cell RNA sequencing of five TNBCs revealed two cancer‐associated fibroblast...

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Vydáno v:The EMBO journal Ročník 39; číslo 19; s. e104063 - n/a
Hlavní autoři: Wu, Sunny Z, Roden, Daniel L, Wang, Chenfei, Holliday, Holly, Harvey, Kate, Cazet, Aurélie S, Murphy, Kendelle J, Pereira, Brooke, Al‐Eryani, Ghamdan, Bartonicek, Nenad, Hou, Rui, Torpy, James R, Junankar, Simon, Chan, Chia‐Ling, Lam, Chuan En, Hui, Mun N, Gluch, Laurence, Beith, Jane, Parker, Andrew, Robbins, Elizabeth, Segara, Davendra, Mak, Cindy, Cooper, Caroline, Warrier, Sanjay, Forrest, Alistair, Powell, Joseph, O'Toole, Sandra, Cox, Thomas R, Timpson, Paul, Lim, Elgene, Liu, X Shirley, Swarbrick, Alexander
Médium: Journal Article
Jazyk:angličtina
Vydáno: London Nature Publishing Group UK 01.10.2020
Springer Nature B.V
John Wiley and Sons Inc
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ISSN:0261-4189, 1460-2075, 1460-2075
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Abstract The tumour stroma regulates nearly all stages of carcinogenesis. Stromal heterogeneity in human triple‐negative breast cancers (TNBCs) remains poorly understood, limiting the development of stromal‐targeted therapies. Single‐cell RNA sequencing of five TNBCs revealed two cancer‐associated fibroblast (CAF) and two perivascular‐like (PVL) subpopulations. CAFs clustered into two states: the first with features of myofibroblasts and the second characterised by high expression of growth factors and immunomodulatory molecules. PVL cells clustered into two states consistent with a differentiated and immature phenotype. We showed that these stromal states have distinct morphologies, spatial relationships and functional properties in regulating the extracellular matrix. Using cell signalling predictions, we provide evidence that stromal‐immune crosstalk acts via a diverse array of immunoregulatory molecules. Importantly, the investigation of gene signatures from inflammatory‐CAFs and differentiated‐PVL cells in independent TNBC patient cohorts revealed strong associations with cytotoxic T‐cell dysfunction and exclusion, respectively. Such insights present promising candidates to further investigate for new therapeutic strategies in the treatment of TNBCs. Synopsis This single‐cell gene expression resource deciphers the composition of triple‐negative breast cancer (TNBC) stroma, revealing distinct subclasses of cancer‐associated fibroblasts (CAFs) and perivascular‐like (PVL) cells. These signatures are informative on tumour aetiology and potential strategies for development of targeted therapies. Single‐cell analysis of primary TNBC highlights clusters of stromal and immune cell types. TNBC stroma is comprised of myofibroblast‐like CAFs, inflammatory‐like CAFs, differentiated PVL and immature PVL cells. Stromal subclasses differ in surface markers, spatial localisation in tissue, ECM functions, and predicted cellular crosstalk with immune cells. Inflammatory‐like CAF and differentiated PVL cells are associated with cytotoxic T‐cell dysfunction and exclusion in independent TNBC‐patient cohorts. Graphical Abstract Single‐cell profiling of primary breast cancer provides unprecedented insights into cell‐type heterogeneity within the tumor microenvironment.
AbstractList The tumour stroma regulates nearly all stages of carcinogenesis. Stromal heterogeneity in human triple‐negative breast cancers (TNBCs) remains poorly understood, limiting the development of stromal‐targeted therapies. Single‐cell RNA sequencing of five TNBCs revealed two cancer‐associated fibroblast (CAF) and two perivascular‐like (PVL) subpopulations. CAFs clustered into two states: the first with features of myofibroblasts and the second characterised by high expression of growth factors and immunomodulatory molecules. PVL cells clustered into two states consistent with a differentiated and immature phenotype. We showed that these stromal states have distinct morphologies, spatial relationships and functional properties in regulating the extracellular matrix. Using cell signalling predictions, we provide evidence that stromal‐immune crosstalk acts via a diverse array of immunoregulatory molecules. Importantly, the investigation of gene signatures from inflammatory‐CAFs and differentiated‐PVL cells in independent TNBC patient cohorts revealed strong associations with cytotoxic T‐cell dysfunction and exclusion, respectively. Such insights present promising candidates to further investigate for new therapeutic strategies in the treatment of TNBCs. Single‐cell profiling of primary breast cancer provides unprecedented insights into cell‐type heterogeneity within the tumor microenvironment.
The tumour stroma regulates nearly all stages of carcinogenesis. Stromal heterogeneity in human triple-negative breast cancers (TNBCs) remains poorly understood, limiting the development of stromal-targeted therapies. Single-cell RNA sequencing of five TNBCs revealed two cancer-associated fibroblast (CAF) and two perivascular-like (PVL) subpopulations. CAFs clustered into two states: the first with features of myofibroblasts and the second characterised by high expression of growth factors and immunomodulatory molecules. PVL cells clustered into two states consistent with a differentiated and immature phenotype. We showed that these stromal states have distinct morphologies, spatial relationships and functional properties in regulating the extracellular matrix. Using cell signalling predictions, we provide evidence that stromal-immune crosstalk acts via a diverse array of immunoregulatory molecules. Importantly, the investigation of gene signatures from inflammatory-CAFs and differentiated-PVL cells in independent TNBC patient cohorts revealed strong associations with cytotoxic T-cell dysfunction and exclusion, respectively. Such insights present promising candidates to further investigate for new therapeutic strategies in the treatment of TNBCs.
The tumour stroma regulates nearly all stages of carcinogenesis. Stromal heterogeneity in human triple‐negative breast cancers (TNBCs) remains poorly understood, limiting the development of stromal‐targeted therapies. Single‐cell RNA sequencing of five TNBCs revealed two cancer‐associated fibroblast (CAF) and two perivascular‐like (PVL) subpopulations. CAFs clustered into two states: the first with features of myofibroblasts and the second characterised by high expression of growth factors and immunomodulatory molecules. PVL cells clustered into two states consistent with a differentiated and immature phenotype. We showed that these stromal states have distinct morphologies, spatial relationships and functional properties in regulating the extracellular matrix. Using cell signalling predictions, we provide evidence that stromal‐immune crosstalk acts via a diverse array of immunoregulatory molecules. Importantly, the investigation of gene signatures from inflammatory‐CAFs and differentiated‐PVL cells in independent TNBC patient cohorts revealed strong associations with cytotoxic T‐cell dysfunction and exclusion, respectively. Such insights present promising candidates to further investigate for new therapeutic strategies in the treatment of TNBCs. Synopsis This single‐cell gene expression resource deciphers the composition of triple‐negative breast cancer (TNBC) stroma, revealing distinct subclasses of cancer‐associated fibroblasts (CAFs) and perivascular‐like (PVL) cells. These signatures are informative on tumour aetiology and potential strategies for development of targeted therapies. Single‐cell analysis of primary TNBC highlights clusters of stromal and immune cell types. TNBC stroma is comprised of myofibroblast‐like CAFs, inflammatory‐like CAFs, differentiated PVL and immature PVL cells. Stromal subclasses differ in surface markers, spatial localisation in tissue, ECM functions, and predicted cellular crosstalk with immune cells. Inflammatory‐like CAF and differentiated PVL cells are associated with cytotoxic T‐cell dysfunction and exclusion in independent TNBC‐patient cohorts. Graphical Abstract Single‐cell profiling of primary breast cancer provides unprecedented insights into cell‐type heterogeneity within the tumor microenvironment.
The tumour stroma regulates nearly all stages of carcinogenesis. Stromal heterogeneity in human triple-negative breast cancers (TNBCs) remains poorly understood, limiting the development of stromal-targeted therapies. Single-cell RNA sequencing of five TNBCs revealed two cancer-associated fibroblast (CAF) and two perivascular-like (PVL) subpopulations. CAFs clustered into two states: the first with features of myofibroblasts and the second characterised by high expression of growth factors and immunomodulatory molecules. PVL cells clustered into two states consistent with a differentiated and immature phenotype. We showed that these stromal states have distinct morphologies, spatial relationships and functional properties in regulating the extracellular matrix. Using cell signalling predictions, we provide evidence that stromal-immune crosstalk acts via a diverse array of immunoregulatory molecules. Importantly, the investigation of gene signatures from inflammatory-CAFs and differentiated-PVL cells in independent TNBC patient cohorts revealed strong associations with cytotoxic T-cell dysfunction and exclusion, respectively. Such insights present promising candidates to further investigate for new therapeutic strategies in the treatment of TNBCs.The tumour stroma regulates nearly all stages of carcinogenesis. Stromal heterogeneity in human triple-negative breast cancers (TNBCs) remains poorly understood, limiting the development of stromal-targeted therapies. Single-cell RNA sequencing of five TNBCs revealed two cancer-associated fibroblast (CAF) and two perivascular-like (PVL) subpopulations. CAFs clustered into two states: the first with features of myofibroblasts and the second characterised by high expression of growth factors and immunomodulatory molecules. PVL cells clustered into two states consistent with a differentiated and immature phenotype. We showed that these stromal states have distinct morphologies, spatial relationships and functional properties in regulating the extracellular matrix. Using cell signalling predictions, we provide evidence that stromal-immune crosstalk acts via a diverse array of immunoregulatory molecules. Importantly, the investigation of gene signatures from inflammatory-CAFs and differentiated-PVL cells in independent TNBC patient cohorts revealed strong associations with cytotoxic T-cell dysfunction and exclusion, respectively. Such insights present promising candidates to further investigate for new therapeutic strategies in the treatment of TNBCs.
The tumour stroma regulates nearly all stages of carcinogenesis. Stromal heterogeneity in human triple‐negative breast cancers (TNBCs) remains poorly understood, limiting the development of stromal‐targeted therapies. Single‐cell RNA sequencing of five TNBCs revealed two cancer‐associated fibroblast (CAF) and two perivascular‐like (PVL) subpopulations. CAFs clustered into two states: the first with features of myofibroblasts and the second characterised by high expression of growth factors and immunomodulatory molecules. PVL cells clustered into two states consistent with a differentiated and immature phenotype. We showed that these stromal states have distinct morphologies, spatial relationships and functional properties in regulating the extracellular matrix. Using cell signalling predictions, we provide evidence that stromal‐immune crosstalk acts via a diverse array of immunoregulatory molecules. Importantly, the investigation of gene signatures from inflammatory‐CAFs and differentiated‐PVL cells in independent TNBC patient cohorts revealed strong associations with cytotoxic T‐cell dysfunction and exclusion, respectively. Such insights present promising candidates to further investigate for new therapeutic strategies in the treatment of TNBCs. Synopsis This single‐cell gene expression resource deciphers the composition of triple‐negative breast cancer (TNBC) stroma, revealing distinct subclasses of cancer‐associated fibroblasts (CAFs) and perivascular‐like (PVL) cells. These signatures are informative on tumour aetiology and potential strategies for development of targeted therapies. Single‐cell analysis of primary TNBC highlights clusters of stromal and immune cell types. TNBC stroma is comprised of myofibroblast‐like CAFs, inflammatory‐like CAFs, differentiated PVL and immature PVL cells. Stromal subclasses differ in surface markers, spatial localisation in tissue, ECM functions, and predicted cellular crosstalk with immune cells. Inflammatory‐like CAF and differentiated PVL cells are associated with cytotoxic T‐cell dysfunction and exclusion in independent TNBC‐patient cohorts. Single‐cell profiling of primary breast cancer provides unprecedented insights into cell‐type heterogeneity within the tumor microenvironment.
Author Forrest, Alistair
Robbins, Elizabeth
Torpy, James R
Mak, Cindy
Cox, Thomas R
Lim, Elgene
Bartonicek, Nenad
Parker, Andrew
Liu, X Shirley
Chan, Chia‐Ling
Murphy, Kendelle J
Powell, Joseph
Roden, Daniel L
Holliday, Holly
Hou, Rui
Beith, Jane
Lam, Chuan En
Cooper, Caroline
Junankar, Simon
Timpson, Paul
Al‐Eryani, Ghamdan
Wang, Chenfei
Pereira, Brooke
Cazet, Aurélie S
O'Toole, Sandra
Harvey, Kate
Swarbrick, Alexander
Hui, Mun N
Gluch, Laurence
Warrier, Sanjay
Segara, Davendra
Wu, Sunny Z
AuthorAffiliation 8 St Vincent's Hospital Darlinghurst NSW Australia
3 Department of Data Sciences Center for Functional Cancer Epigenetics Dana‐Farber Cancer Institute Harvard T.H. Chan School of Public Health Boston MA USA
11 Southside Clinical Unit Faculty of Medicine University of Queensland Brisbane Qld Australia
12 Department of Breast Surgery Chris O'Brien Lifehouse Camperdown NSW Australia
16 Australian Clinical Laboratories Northern Beaches Hospital Frenchs Forest NSW Australia
6 Chris O'Brien Lifehouse Camperdown NSW Australia
15 UNSW Cellular Genomics Futures Institute University of New South Wales Sydney NSW Australia
13 Royal Prince Alfred Institute of Academic Surgery Sydney University Sydney NSW Australia
7 The Strathfield Breast Centre Strathfield NSW Australia
2 St Vincent's Clinical School Faculty of Medicine UNSW Sydney Sydney NSW Australia
5 Garvan‐Weizmann Centre for Cellular Genomics Garvan Institute of Medical Research Sydney NSW Australia
14 RIKEN Center for Integrative Medical Sciences Yok
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– name: 15 UNSW Cellular Genomics Futures Institute University of New South Wales Sydney NSW Australia
– name: 2 St Vincent's Clinical School Faculty of Medicine UNSW Sydney Sydney NSW Australia
– name: 10 Pathology Queensland Princess Alexandra Hospital Brisbane Qld Australia
– name: 13 Royal Prince Alfred Institute of Academic Surgery Sydney University Sydney NSW Australia
– name: 16 Australian Clinical Laboratories Northern Beaches Hospital Frenchs Forest NSW Australia
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– name: 6 Chris O'Brien Lifehouse Camperdown NSW Australia
– name: 7 The Strathfield Breast Centre Strathfield NSW Australia
– name: 14 RIKEN Center for Integrative Medical Sciences Yokohama Japan
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– name: 4 Harry Perkins Institute of Medical Research QEII Medical Centre and Centre for Medical Research The University of Western Australia Nedlands, Perth WA Australia
– name: 8 St Vincent's Hospital Darlinghurst NSW Australia
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  givenname: Daniel L
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  givenname: Chenfei
  surname: Wang
  fullname: Wang, Chenfei
  organization: Department of Data Sciences, Center for Functional Cancer Epigenetics, Dana‐Farber Cancer Institute, Harvard T.H. Chan School of Public Health
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  givenname: Holly
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  givenname: Rui
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  givenname: Thomas R
  orcidid: 0000-0001-9294-1745
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  givenname: Elgene
  surname: Lim
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  organization: The Kinghorn Cancer Centre and Cancer Research Division, Garvan Institute of Medical Research, St Vincent's Clinical School, Faculty of Medicine, UNSW Sydney, St Vincent's Hospital
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  surname: Liu
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  organization: Department of Data Sciences, Center for Functional Cancer Epigenetics, Dana‐Farber Cancer Institute, Harvard T.H. Chan School of Public Health
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  orcidid: 0000-0002-3051-5676
  surname: Swarbrick
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  email: a.swarbrick@garvan.org.au
  organization: The Kinghorn Cancer Centre and Cancer Research Division, Garvan Institute of Medical Research, St Vincent's Clinical School, Faculty of Medicine, UNSW Sydney
BackLink https://www.ncbi.nlm.nih.gov/pubmed/32790115$$D View this record in MEDLINE/PubMed
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Keywords tumour microenvironment
cancer‐associated fibroblasts
triple‐negative breast cancer
stromal heterogeneity
single‐cell RNA sequencing
single-cell RNA sequencing
cancer-associated fibroblasts
triple-negative breast cancer
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Snippet The tumour stroma regulates nearly all stages of carcinogenesis. Stromal heterogeneity in human triple‐negative breast cancers (TNBCs) remains poorly...
The tumour stroma regulates nearly all stages of carcinogenesis. Stromal heterogeneity in human triple-negative breast cancers (TNBCs) remains poorly...
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StartPage e104063
SubjectTerms Breast cancer
cancer‐associated fibroblasts
Carcinogenesis
Carcinogens
Cell differentiation
Crosstalk
Cytotoxicity
Development strategies
EMBO03
EMBO19
Extracellular matrix
Extracellular Matrix - immunology
Extracellular Matrix - pathology
Female
Fibroblasts
Gene expression
Gene sequencing
Growth factors
Heterogeneity
Humans
Immune evasion
Immune system
Immunomodulation
Immunomodulators
Immunoregulation
Inflammation
Phenotypes
Resource
Ribonucleic acid
RNA
RNA-Seq
Signatures
single‐cell RNA sequencing
Stromal Cells - immunology
Stromal Cells - pathology
stromal heterogeneity
Subpopulations
Surface markers
T-Lymphocytes, Cytotoxic - immunology
T-Lymphocytes, Cytotoxic - pathology
Triple Negative Breast Neoplasms - immunology
Triple Negative Breast Neoplasms - pathology
triple‐negative breast cancer
Tumor Escape
Tumors
tumour microenvironment
Title Stromal cell diversity associated with immune evasion in human triple‐negative breast cancer
URI https://link.springer.com/article/10.15252/embj.2019104063
https://onlinelibrary.wiley.com/doi/abs/10.15252%2Fembj.2019104063
https://www.ncbi.nlm.nih.gov/pubmed/32790115
https://www.proquest.com/docview/2447473819
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https://pubmed.ncbi.nlm.nih.gov/PMC7527929
Volume 39
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