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Book: HSF1 and molecular chaperones in biology and cancer

Mendillo, Marc Laurence / Pincus, David / Scherz-Shouval, Ruth

(Advances in experimental medicine and biology ; 1243)

2020

Author's details	Marc Laurence Mendillo,David Pincus, Ruth Scherz-Shouval editors
Series title	Advances in experimental medicine and biology ; 1243
Collection
Language	English
Size	viii, 182 Seiten, Illustrationen
Publisher	Springer
Publishing place	Cham
Publishing country	Switzerland
Document type	Book
HBZ-ID	HT020437102
ISBN	978-3-030-40203-7 ; 9783030402044 ; 3-030-40203-7 ; 3030402045
Database	Catalogue ZB MED Medicine, Health

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Article ; Online: Insights into the co-evolution of epithelial cells and fibroblasts in the esophageal tumor microenvironment.

Lavon, Hagar / Scherz-Shouval, Ruth

Cancer cell

2023 Volume 41, Issue 5, Page(s) 826–828

Abstract: Cancer-associated fibroblasts (CAFs) are recruited and rewired by cancer cells to become protumorigenic. The molecular mechanisms underlying this crosstalk in esophageal cancer are completely unknown. Chen et al. discover that premalignant epithelial ... ...

Abstract	Cancer-associated fibroblasts (CAFs) are recruited and rewired by cancer cells to become protumorigenic. The molecular mechanisms underlying this crosstalk in esophageal cancer are completely unknown. Chen et al. discover that premalignant epithelial cells of the esophagus rewire normal resident fibroblasts into CAFs through the downregulation of ANXA1-FRP2 signaling.
MeSH term(s)	Humans ; Tumor Microenvironment ; Esophageal Neoplasms/genetics ; Fibroblasts ; Epithelial Cells
Language	English
Publishing date	2023-04-12
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2023.03.020
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Zs.A 5650: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 104: Show issues

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Article ; Online: From gatekeepers to providers: regulation of immune functions by cancer-associated fibroblasts.

Arpinati, Ludovica / Scherz-Shouval, Ruth

Trends in cancer

2023 Volume 9, Issue 5, Page(s) 421–443

Abstract: Cancer-associated fibroblasts (CAFs) are major protumorigenic components of the tumor microenvironment in solid cancers. CAFs are heterogeneous, consisting of multiple subsets that display diverse functions. Recently, CAFs have emerged as major promoters ...

Abstract	Cancer-associated fibroblasts (CAFs) are major protumorigenic components of the tumor microenvironment in solid cancers. CAFs are heterogeneous, consisting of multiple subsets that display diverse functions. Recently, CAFs have emerged as major promoters of immune evasion. CAFs favor T cell exclusion and exhaustion, promote recruitment of myeloid-derived suppressor cells, and induce protumoral phenotypic shifts in macrophages and neutrophils. With the growing appreciation of CAF heterogeneity came the understanding that different CAF subpopulations may be driving distinct immune-regulatory effects, interacting with different cell types, and perhaps even driving opposing effects on malignancy. In this review we discuss the current understanding of CAF-immune interactions, their effect on tumor progression and therapeutic response, and the possibility of exploiting CAF-immune interactions as potential targets for cancer therapy.
MeSH term(s)	Humans ; Cancer-Associated Fibroblasts/pathology ; Neoplasms/genetics ; Neoplasms/therapy ; Neoplasms/metabolism ; Macrophages/metabolism ; T-Lymphocytes ; Immunity ; Tumor Microenvironment
Language	English
Publishing date	2023-03-02
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2852626-0
ISSN	2405-8025 ; 2405-8033 ; 2405-8033
ISSN (online)	2405-8025 ; 2405-8033
ISSN	2405-8033
DOI	10.1016/j.trecan.2023.01.007
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Article ; Online: Unlocking the Role of Age-Related Changes to Fibroblasts in Pancreatic Cancer.

Isaacson, Achinoam / Barki, Debra / Scherz-Shouval, Ruth

Cancer research

2024 Volume 84, Issue 8, Page(s) 1185–1187

Abstract: Pancreatic cancer prevalence increases with age, and disease prognosis is poorer in older individuals. The increased prevalence is driven, undoubtedly, by the multistep accumulation of oncogenic mutations in cancer cells with age. However, fibroblasts ... ...

Abstract	Pancreatic cancer prevalence increases with age, and disease prognosis is poorer in older individuals. The increased prevalence is driven, undoubtedly, by the multistep accumulation of oncogenic mutations in cancer cells with age. However, fibroblasts are major constituents and key players in pancreatic cancer, and they too undergo age-related changes that may contribute to disease severity. In this issue of Cancer Research, Zabransky and colleagues set out to dissect the effect of age-related changes in pancreatic fibroblasts on pancreatic ductal adenocarcinoma growth and metastasis. They discovered that aged fibroblasts secrete GDF-15, which in turn activates AKT signaling and accelerates tumor progression. These findings provide a mechanistic role for aged fibroblasts in pancreatic cancer, underpinning the importance of normal physiologic processes in tumor progression. See related article by Zabransky et al., p. 1221.
MeSH term(s)	Humans ; Aged ; Pancreatic Neoplasms/genetics ; Carcinoma, Pancreatic Ductal/genetics ; Pancreas ; Fibroblasts ; Signal Transduction
Language	English
Publishing date	2024-03-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-24-0439
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Article ; Online: Keeping IPMNs in Check: A Novel Role for the Transcription Factor NKX6-2 in Preserving an Indolent Cell Identity in Pancreatic Cystic Lesions.

Ben-Shmuel, Aviad / Scherz-Shouval, Ruth

Cancer discovery

2023 Volume 13, Issue 8, Page(s) 1768–1770

Abstract: Summary: In this issue of Cancer Discovery, Sans and colleagues identify the transcription factor NKX6-2 as a principal element in maintaining the low-grade gastric cell phenotype of intraductal papillary mucinous neoplasms (IPMN) in the pancreas. Their ...

Abstract	Summary: In this issue of Cancer Discovery, Sans and colleagues identify the transcription factor NKX6-2 as a principal element in maintaining the low-grade gastric cell phenotype of intraductal papillary mucinous neoplasms (IPMN) in the pancreas. Their discoveries in patient cohorts and dissection in animal models provide a novel molecular understanding underpinning IPMN differentiation, with implications for risk stratification and therapeutic intervention in pancreatic cancer. See related article by Sans et al., p. 1844 (7).
MeSH term(s)	Animals ; Pancreatic Intraductal Neoplasms ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/pathology ; Transcriptome ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; Pancreas/pathology ; Pancreatic Cyst/genetics ; Cell Differentiation ; Transcription Factors/genetics
Chemical Substances	Transcription Factors
Language	English
Publishing date	2023-07-19
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-23-0590
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Zs.A 6916: Show issues

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Article ; Online: Cancer-associated fibroblasts in the single-cell era.

Lavie, Dor / Ben-Shmuel, Aviad / Erez, Neta / Scherz-Shouval, Ruth

Nature cancer

2022 Volume 3, Issue 7, Page(s) 793–807

Abstract: Cancer-associated fibroblasts (CAFs) are central players in the microenvironment of solid tumors, affecting cancer progression and metastasis. CAFs have diverse phenotypes, origins and functions and consist of distinct subpopulations. Recent progress in ... ...

Abstract	Cancer-associated fibroblasts (CAFs) are central players in the microenvironment of solid tumors, affecting cancer progression and metastasis. CAFs have diverse phenotypes, origins and functions and consist of distinct subpopulations. Recent progress in single-cell RNA-sequencing technologies has enabled detailed characterization of the complexity and heterogeneity of CAF subpopulations in multiple tumor types. In this Review, we discuss the current understanding of CAF subsets and functions as elucidated by single-cell technologies, their functional plasticity, and their emergent shared and organ-specific features that could potentially be harnessed to design better therapeutic strategies for cancer.
MeSH term(s)	Cancer-Associated Fibroblasts/pathology ; Humans ; Neoplasms/genetics ; Tumor Microenvironment/genetics
Language	English
Publishing date	2022-07-26
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ISSN	2662-1347
ISSN (online)	2662-1347
DOI	10.1038/s43018-022-00411-z
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Article: The Role of HSF1 and the Chaperone Network in the Tumor Microenvironment.

Grunberg, Nil / Levi-Galibov, Oshrat / Scherz-Shouval, Ruth

Advances in experimental medicine and biology

2020 Volume 1243, Page(s) 101–111

Abstract: Tumors are stressful environments. As tumors evolve from single mutated cancer cells into invasive malignancies they must overcome various constraints and barriers imposed by a hostile microenvironment. To achieve this, cancer cells recruit and rewire ... ...

Abstract	Tumors are stressful environments. As tumors evolve from single mutated cancer cells into invasive malignancies they must overcome various constraints and barriers imposed by a hostile microenvironment. To achieve this, cancer cells recruit and rewire cells in their microenvironment to become pro-tumorigenic. We propose that chaperones are vital players in this process, and that activation of stress responses helps tumors adapt and evolve into aggressive malignancies, by enabling phenotypic plasticity in the tumor microenvironment (TME). In this chapter we will review evidence supporting non-cancer-cell-autonomous activity of chaperones in human patients and mouse models of cancer, discuss the mechanisms by which this non-cell-autonomous activity is mediated and provide an evolutionary perspective on the basis of this phenomenon.
MeSH term(s)	Animals ; Carcinogenesis ; Heat Shock Transcription Factors/metabolism ; Humans ; Molecular Chaperones/metabolism ; Neoplasms/genetics ; Neoplasms/metabolism ; Tumor Microenvironment/genetics
Chemical Substances	HSF1 protein, human ; Heat Shock Transcription Factors ; Molecular Chaperones
Language	English
Publishing date	2020-04-15
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-3-030-40204-4_7
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Article ; Online: Loss of EIF4G2 mediates aggressiveness in distinct human endometrial cancer subpopulations with poor survival outcome in patients.

Meril, Sara / Muhlbauer Avni, Maya / Lior, Chen / Bahlsen, Marcela / Olender, Tsviya / Savidor, Alon / Krausz, Judit / Belhanes Peled, Hila / Birisi, Hila / David, Nofar / Bialik, Shani / Scherz-Shouval, Ruth / Ben David, Yehuda / Kimchi, Adi

Oncogene

2024 Volume 43, Issue 15, Page(s) 1098–1112

Abstract: The non-canonical translation initiation factor EIF4G2 plays essential roles in cellular stress responses via translation of selective mRNA cohorts. Currently there is limited and conflicting information regarding its involvement in cancer development ... ...

Abstract	The non-canonical translation initiation factor EIF4G2 plays essential roles in cellular stress responses via translation of selective mRNA cohorts. Currently there is limited and conflicting information regarding its involvement in cancer development and progression. Here we assessed its role in endometrial cancer (EC), in a cohort of 280 EC patients across different types, grades, and stages, and found that low EIF4G2 expression highly correlated with poor overall- and recurrence-free survival in Grade 2 EC patients, monitored over a period of up to 12 years. To establish a causative connection between low EIF4G2 expression and cancer progression, we stably knocked-down EIF4G2 in two human EC cell lines in parallel. EIF4G2 depletion resulted in increased resistance to conventional therapies and increased the prevalence of molecular markers for aggressive cell subsets, altering their transcriptional and proteomic landscapes. Prominent among the proteins with decreased abundance were Kinesin-1 motor proteins, KIF5B and KLC1, 2, 3. Multiplexed imaging of the EC patient tumor cohort showed a correlation between decreased expression of the kinesin proteins, and poor survival in patients with tumors of certain grades and stages. These findings reveal potential novel biomarkers for Grade 2 EC with ramifications for patient stratification and therapeutic interventions.
MeSH term(s)	Female ; Humans ; Kinesins/genetics ; Proteomics ; Cell Line ; Endometrial Neoplasms/genetics ; Endometrial Neoplasms/pathology ; Eukaryotic Initiation Factor-4G/genetics ; Eukaryotic Initiation Factor-4G/metabolism
Chemical Substances	Kinesins (EC 3.6.4.4) ; EIF4G2 protein, human ; Eukaryotic Initiation Factor-4G
Language	English
Publishing date	2024-02-22
Publishing country	England
Document type	Journal Article
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-024-02981-x
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Article ; Online: Global DNA Methylation Analysis of Cancer-Associated Fibroblasts Reveals Extensive Epigenetic Rewiring Linked with RUNX1 Upregulation in Breast Cancer Stroma.

Halperin, Coral / Hey, Joschka / Weichenhan, Dieter / Stein, Yaniv / Mayer, Shimrit / Lutsik, Pavlo / Plass, Christoph / Scherz-Shouval, Ruth

Cancer research

2022 Volume 82, Issue 22, Page(s) 4139–4152

Abstract: Cancer cells recruit and rewire normal fibroblasts in their microenvironment to become protumorigenic cancer-associated fibroblasts (CAF). These CAFs are genomically stable, yet their transcriptional programs are distinct from those of their normal ... ...

Abstract	Cancer cells recruit and rewire normal fibroblasts in their microenvironment to become protumorigenic cancer-associated fibroblasts (CAF). These CAFs are genomically stable, yet their transcriptional programs are distinct from those of their normal counterparts. Transcriptional regulation plays a major role in this reprogramming, but the extent to which epigenetic modifications of DNA also contribute to the rewiring of CAF transcription is not clear. Here we address this question by dissecting the epigenetic landscape of breast CAFs. Applying tagmentation-based whole-genome bisulfite sequencing in a mouse model of breast cancer, we found that fibroblasts undergo massive DNA methylation changes as they transition into CAFs. Transcriptional and epigenetic analyses revealed RUNX1 as a potential mediator of this process and identified a RUNX1-dependent stromal gene signature. Coculture and mouse models showed that both RUNX1 and its stromal signature are induced as normal fibroblasts transition into CAFs. In breast cancer patients, RUNX1 was upregulated in CAFs, and expression of the RUNX1 signature was associated with poor disease outcome, highlighting the relevance of these findings to human disease. This work presents a comprehensive genome-wide map of DNA methylation in CAFs and reveals a previously unknown facet of the dynamic plasticity of the stroma. Significance: The first genome-wide map of DNA methylation in breast cancer-associated fibroblasts unravels a previously unknown facet of the dynamic plasticity of the stroma, with far-reaching therapeutic implications.
MeSH term(s)	Humans ; Mice ; Animals ; Female ; Cancer-Associated Fibroblasts/metabolism ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; DNA Methylation ; Up-Regulation ; Core Binding Factor Alpha 2 Subunit/genetics ; Core Binding Factor Alpha 2 Subunit/metabolism ; Fibroblasts/metabolism ; Epigenesis, Genetic ; Tumor Microenvironment/genetics
Chemical Substances	Core Binding Factor Alpha 2 Subunit ; RUNX1 protein, human ; Runx1 protein, mouse
Language	English
Publishing date	2022-10-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-22-0209
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Article ; Online: DNA methylation landscape of tumor-associated macrophages reveals pathways, transcription factors and prognostic value relevant to triple-negative breast cancer patients.

Hey, Joschka / Halperin, Coral / Hartmann, Mark / Mayer, Shimrit / Schönung, Maximilian / Lipka, Daniel B / Scherz-Shouval, Ruth / Plass, Christoph

International journal of cancer

2022 Volume 152, Issue 6, Page(s) 1226–1242

Abstract: The accumulation of myeloid cells, particularly tumor-associated macrophages (TAMs), characterizes the tumor microenvironment (TME) of many solid cancers, including breast cancer. Compared to healthy tissue-resident macrophages, TAMs acquire distinct ... ...

Abstract	The accumulation of myeloid cells, particularly tumor-associated macrophages (TAMs), characterizes the tumor microenvironment (TME) of many solid cancers, including breast cancer. Compared to healthy tissue-resident macrophages, TAMs acquire distinct transcriptomes and tumor-promoting functions by largely unknown mechanisms. Here, we hypothesize the involvement of TME signaling and subsequent epigenetic reprogramming of TAMs. Using the 4T1 mouse model of triple-negative breast cancer, we demonstrate that the presence of cancer cells significantly alters the DNA methylation landscape of macrophages and, to a lesser extent, bone marrow-derived monocytes (BMDMs). TAM methylomes, dissected into BMDM-originating and TAM-specific epigenetic programs, implicated transcription factors (TFs) and signaling pathways involved in TAM reprogramming, correlated with cancer-specific gene expression patterns. Utilizing published single-cell gene expression data, we linked microenvironmentally-derived signals to the cancer-specific DNA methylation landscape of TAMs. These integrative analyses highlighted the role of altered cytokine production in the TME (eg, TGF-β, IFN-γ and CSF1) on the induction of specific TFs (eg, FOSL2, STAT1 and RUNX3) responsible for the epigenetic reprogramming of TAMs. DNA methylation deconvolution identified a TAM-specific signature associated with the identified signaling pathways and TFs, corresponding with severe tumor grade and poor prognosis of breast cancer patients. Similarly, immunosuppressive TAM functions were identified, such as induction of the immune inhibitory receptor-ligand PD-L1 by DNA hypomethylation of Cd274. Collectively, these results provide strong evidence that the epigenetic landscapes of macrophages and monocytes are perturbed by the presence of breast cancer, pointing to molecular mechanisms of TAM reprogramming, impacting patient outcomes.
MeSH term(s)	Humans ; Mice ; Animals ; Triple Negative Breast Neoplasms/genetics ; Prognosis ; Tumor-Associated Macrophages ; Transcription Factors ; DNA Methylation ; Tumor Microenvironment/genetics
Chemical Substances	Transcription Factors
Language	English
Publishing date	2022-12-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218257-9
ISSN	1097-0215 ; 0020-7136
ISSN (online)	1097-0215
ISSN	0020-7136
DOI	10.1002/ijc.34364
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