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Book: The Hippo signaling pathway and cancer

Oren, Moshe / Aylon, Yael

2013

Author's details	Moshe Oren ; Yael Aylon ed
Keywords	Carcinogenesis ; Tumors--Growth
Subject code	616.994071
Language	English
Size	VI, 354 S. : Ill., graph. Darst., 24 cm
Publisher	Springer
Publishing place	New York u.a.
Publishing country	United States
Document type	Book
HBZ-ID	HT017605879
ISBN	978-1-4614-6219-4 ; 1-4614-6219-3 ; 9781461462200 ; 1461462207
Database	Catalogue ZB MED Medicine, Health

In stock of ZB MED Cologne/Königswinter

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2013 A 482	available for loan (reading room)	Lesesaal EG

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Article ; Online: Tumor Suppression by p53: Bring in the Hippo!

Aylon, Yael / Oren, Moshe

Cancer cell

2017 Volume 32, Issue 4, Page(s) 397–399

Abstract: In this issue of Cancer Cell, Mello et al. investigated how p53 suppresses pancreatic cancer and discovered a key role for the tyrosine phosphatase PTPN14, a p53 transcriptional target. PTPN14 restrains YAP, curbing its potential oncogenic effects. The ... ...

Abstract	In this issue of Cancer Cell, Mello et al. investigated how p53 suppresses pancreatic cancer and discovered a key role for the tyrosine phosphatase PTPN14, a p53 transcriptional target. PTPN14 restrains YAP, curbing its potential oncogenic effects. The p53-PTPN14-YAP axis highlights the importance of signaling pathway coordination in cancer prevention.
MeSH term(s)	Humans ; Oncogenes ; Pancreatic Neoplasms ; Phosphoproteins/genetics ; Protein Tyrosine Phosphatases, Non-Receptor/genetics ; Protein-Serine-Threonine Kinases ; Signal Transduction ; Tumor Suppressor Protein p53
Chemical Substances	Phosphoproteins ; Tumor Suppressor Protein p53 ; Hippo protein, human (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; PTPN14 protein, human (EC 3.1.3.48) ; Protein Tyrosine Phosphatases, Non-Receptor (EC 3.1.3.48)
Language	English
Publishing date	2017-10-06
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.2017.09.010
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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: ATF3 characterizes aggressive drug-tolerant persister cells in HGSOC.

Böpple, Kathrin / Oren, Yaara / Henry, Whitney S / Dong, Meng / Weller, Sandra / Thiel, Julia / Kleih, Markus / Gaißler, Andrea / Zipperer, Damaris / Kopp, Hans-Georg / Aylon, Yael / Oren, Moshe / Essmann, Frank / Liang, Chunguang / Aulitzky, Walter E

Cell death & disease

2024 Volume 15, Issue 4, Page(s) 290

Abstract: High-grade serous ovarian cancer (HGSOC) represents the most common and lethal subtype of ovarian cancer. Despite initial response to platinum-based standard therapy, patients commonly suffer from relapse that likely originates from drug-tolerant ... ...

Abstract	High-grade serous ovarian cancer (HGSOC) represents the most common and lethal subtype of ovarian cancer. Despite initial response to platinum-based standard therapy, patients commonly suffer from relapse that likely originates from drug-tolerant persister (DTP) cells. We generated isogenic clones of treatment-naïve and cisplatin-tolerant persister HGSOC cells. In addition, single-cell RNA sequencing of barcoded cells was performed in a xenograft model with HGSOC cell lines after platinum-based therapy. Published single-cell RNA-sequencing data from neo-adjuvant and non-treated HGSOC patients and patient data from TCGA were analyzed. DTP-derived cells exhibited morphological alterations and upregulation of epithelial-mesenchymal transition (EMT) markers. An aggressive subpopulation of DTP-derived cells showed high expression of the stress marker ATF3. Knockdown of ATF3 enhanced the sensitivity of aggressive DTP-derived cells to cisplatin-induced cell death, implying a role for ATF3 stress response in promoting a drug tolerant persister cell state. Furthermore, single cell lineage tracing to detect transcriptional changes in a HGSOC cell line-derived xenograft relapse model showed that cells derived from relapsed solid tumors express increased levels of EMT and multiple endoplasmic reticulum (ER) stress markers, including ATF3. Single cell RNA sequencing of epithelial cells from four HGSOC patients also identified a small cell population resembling DTP cells in all samples. Moreover, analysis of TCGA data from 259 HGSOC patients revealed a significant progression-free survival advantage for patients with low expression of the ATF3-associated partial EMT genes. These findings suggest that increased ATF3 expression together with partial EMT promote the development of aggressive DTP, and thereby relapse in HGSOC patients.
MeSH term(s)	Humans ; Activating Transcription Factor 3/metabolism ; Activating Transcription Factor 3/genetics ; Female ; Cisplatin/pharmacology ; Cisplatin/therapeutic use ; Cell Line, Tumor ; Drug Resistance, Neoplasm/genetics ; Drug Resistance, Neoplasm/drug effects ; Epithelial-Mesenchymal Transition/drug effects ; Epithelial-Mesenchymal Transition/genetics ; Ovarian Neoplasms/drug therapy ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/pathology ; Ovarian Neoplasms/metabolism ; Animals ; Mice ; Xenograft Model Antitumor Assays ; Gene Expression Regulation, Neoplastic/drug effects
Chemical Substances	Activating Transcription Factor 3 ; Cisplatin (Q20Q21Q62J) ; ATF3 protein, human
Language	English
Publishing date	2024-04-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-024-06674-x
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The LATS1 and LATS2 tumor suppressors: beyond the Hippo pathway.

Furth, Noa / Aylon, Yael

Cell death and differentiation

2017 Volume 24, Issue 9, Page(s) 1488–1501

Abstract: Proper cellular functionality and homeostasis are maintained by the convergent integration of various signaling cascades, which enable cells to respond to internal and external changes. The Dbf2-related kinases LATS1 and LATS2 (LATS) have emerged as ... ...

Abstract	Proper cellular functionality and homeostasis are maintained by the convergent integration of various signaling cascades, which enable cells to respond to internal and external changes. The Dbf2-related kinases LATS1 and LATS2 (LATS) have emerged as central regulators of cell fate, by modulating the functions of numerous oncogenic or tumor suppressive effectors, including the canonical Hippo effectors YAP/TAZ, the Aurora mitotic kinase family, estrogen signaling and the tumor suppressive transcription factor p53. While the basic functions of the LATS kinase module are strongly conserved over evolution, the genomic duplication event leading to the emergence of two closely related kinases in higher organisms has increased the complexity of this signaling network. Here, we review the LATS1 and LATS2 intrinsic features as well as their reported cellular activities, emphasizing unique characteristics of each kinase. While differential activities between the two paralogous kinases have been reported, many converge to similar pathways and outcomes. Interestingly, the regulatory networks controlling the mRNA expression pattern of LATS1 and LATS2 differ strongly, and may contribute to the differences in protein binding partners of each kinase and in the subcellular locations in which each kinase exerts its functions.
MeSH term(s)	Animals ; Apoptosis/genetics ; Apoptosis/physiology ; Gene Expression Regulation/genetics ; Gene Expression Regulation/physiology ; Humans ; Phosphorylation/genetics ; Phosphorylation/physiology ; Protein Processing, Post-Translational/genetics ; Protein Processing, Post-Translational/physiology ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; Signal Transduction ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism
Chemical Substances	Tumor Suppressor Proteins ; LATS1 protein, human (EC 2.7.1.-) ; LATS2 protein, human (EC 2.7.1.11) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2017-06-23
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/cdd.2017.99
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Article ; Online: The Paradox of p53: What, How, and Why?

Aylon, Yael / Oren, Moshe

Cold Spring Harbor perspectives in medicine

2016 Volume 6, Issue 10

Abstract: Unlike the rather stereotypic image by which it was portrayed until not too many years ago, p53 is now increasingly emerging as a multifaceted transcription factor that can sometimes exert opposing effects on biological processes. This includes pro- ... ...

Abstract	Unlike the rather stereotypic image by which it was portrayed until not too many years ago, p53 is now increasingly emerging as a multifaceted transcription factor that can sometimes exert opposing effects on biological processes. This includes pro-survival activities that seem to contradict p53's canonical proapoptotic features, as well as opposing effects on cell migration, metabolism, and differentiation. Such antagonistic bifunctionality (balancing both positive and negative signals) bestows p53 with an ideal attribute to govern homeostasis. The molecular mechanisms underpinning the paradoxical activities of p53 may be related to a protein conformational spectrum (from canonical wild-type to "pseudomutant"), diversity of DNA response elements, and/or higher-order chromatin configuration. Altogether, this functional flexibility positions p53 as a transcriptional "super hub" that dictates cell homeostasis, and ultimately cell fate, by governing a hierarchy of other functional hubs. Deciphering the mechanisms by which p53 determines which hubs to engage, and how one might modulate the preferences of p53, remains a major challenge for both basic science and translational cancer medicine.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Apoptosis ; Drug Design ; Gene Expression Regulation ; Humans ; Models, Biological ; Mutation ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Transcriptional Activation ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/physiology
Chemical Substances	Antineoplastic Agents ; Tumor Suppressor Protein p53
Language	English
Publishing date	2016-10-03
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2157-1422
ISSN (online)	2157-1422
DOI	10.1101/cshperspect.a026328
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The Hippo pathway, p53 and cholesterol.

Aylon, Yael / Oren, Moshe

Cell cycle (Georgetown, Tex.)

2016 Volume 15, Issue 17, Page(s) 2248–2255

Abstract: ASBTRACT Increased rates of cholesterol and lipid synthesis have long been recognized as important aspects of the metabolic rewiring that occurs during cancerous transformation. Many genes encoding enzymes involved in cholesterol and fatty acid ... ...

Abstract	ASBTRACT Increased rates of cholesterol and lipid synthesis have long been recognized as important aspects of the metabolic rewiring that occurs during cancerous transformation. Many genes encoding enzymes involved in cholesterol and fatty acid biogenesis are transcriptional targets of the sterol regulatory element-binding proteins (SREBPs). The SREBPs act as a hub for metabolic and proliferation-related signals; their activity is the focus of a tug-of-war between tumor suppressors, who generally inhibit SREBP function, and oncogenes, who often promote, and rely on, SREBP activity. The Hippo pathway plays a central role in coordinating cell proliferation and organ size, whereas p53 is a crucial tumor suppressor that maintains metabolic homeostasis and orchestrates cellular stress responses. Together, the Hippo and p53 signaling pathways cooperate on multiple levels to fine-tune SREPB activity and regulate cholesterol/lipid levels. Cholesterol biosynthesis inhibitors such as statins are appealing conceptually, but have yet to show an indisputable effect on cancer development. Fortunately, the complex regulation surrounding the Hippo-p53-SREBP network potentially provides a broad interface for additional novel cancer-targeting interventions.
MeSH term(s)	Animals ; Cholesterol/metabolism ; Humans ; Models, Biological ; Neoplasms/metabolism ; Neoplasms/therapy ; Protein Serine-Threonine Kinases/metabolism ; Signal Transduction ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Tumor Suppressor Protein p53 ; Cholesterol (97C5T2UQ7J) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2016-07-15
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.1080/15384101.2016.1207840
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Zs.A 5881: Show issues

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Article ; Online: TAZ facilitates breast tumor growth by promoting an immune-suppressive tumor microenvironment.

Gershoni, Anat / Hassin, Ori / Nataraj, Nishanth Belugali / Baruch, Sivan / Avioz-Seligman, Adi / Pirona, Anna Chiara / Fellus-Alyagor, Liat / Meir Salame, Tomer / Mukherjee, Saptaparna / Mallel, Giuseppe / Yarden, Yosef / Aylon, Yael / Oren, Moshe

Molecular oncology

2023 Volume 17, Issue 12, Page(s) 2675–2693

Abstract: The core Hippo pathway module consists of a tumour-suppressive kinase cascade that inhibits the transcriptional coactivators Yes-associated protein (YAP) and WW domain-containing transcription regulator protein 1 (WWTR1; also known as TAZ). When the ... ...

Abstract	The core Hippo pathway module consists of a tumour-suppressive kinase cascade that inhibits the transcriptional coactivators Yes-associated protein (YAP) and WW domain-containing transcription regulator protein 1 (WWTR1; also known as TAZ). When the Hippo pathway is downregulated, as often occurs in breast cancer, YAP/TAZ activity is induced. To elaborate the roles of TAZ in triple-negative breast cancer (TNBC), we depleted Taz in murine TNBC 4T1 cells, using either CRISPR/Cas9 or small hairpin RNA (shRNA). TAZ-depleted cells and their controls, harbouring wild-type levels of TAZ, were orthotopically injected into the mammary fat pads of syngeneic BALB/c female mice, and mice were monitored for tumour growth. TAZ depletion resulted in smaller tumours compared to the tumours generated by control cells, in line with the notion that TAZ functions as an oncogene in breast cancer. Tumours, as well as their corresponding in vitro cultured cells, were then subjected to gene expression profiling by RNA sequencing (RNA-seq). Interestingly, pathway analysis of the RNA-seq data indicated a TAZ-dependent enrichment of 'Inflammatory Response', a pathway correlated with TAZ expression levels also in human breast cancer tumours. Specifically, the RNA-seq analysis predicted a significant depletion of regulatory T cells (Tregs) in TAZ-deficient tumours, which was experimentally validated by the staining of tumour sections and by quantitative cytometry by time of flight (CyTOF). Strikingly, the differences in tumour size were completely abolished in immune-deficient mice, demonstrating that the immune-modulatory capacity of TAZ is critical for its oncogenic activity in this setting. Cytokine array analysis of conditioned medium from cultured cells revealed that TAZ increased the abundance of a small group of cytokines, including plasminogen activator inhibitor 1 (Serpin E1; also known as PAI-1), CCN family member 4 (CCN4; also known as WISP-1) and interleukin-23 (IL-23), suggesting a potential mechanistic explanation for its in vivo immunomodulatory effect. Together, our results imply that TAZ functions in a non-cell-autonomous manner to modify the tumour immune microenvironment and dampen the anti-tumour immune response, thereby facilitating tumour growth.
MeSH term(s)	Animals ; Female ; Humans ; Mice ; Hippo Signaling Pathway ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Transcription Factors/metabolism ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/pathology ; Tumor Microenvironment ; Transcriptional Coactivator with PDZ-Binding Motif Proteins/metabolism
Chemical Substances	Intracellular Signaling Peptides and Proteins ; Transcription Factors ; WWTR1 protein, human ; Transcriptional Coactivator with PDZ-Binding Motif Proteins
Language	English
Publishing date	2023-10-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	2415106-3
ISSN	1878-0261 ; 1574-7891
ISSN (online)	1878-0261
ISSN	1574-7891
DOI	10.1002/1878-0261.13525
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Book: The hippo signaling pathway and cancer

Oren, Moshe / Aylon, Yael

2013

Author's details	Moshe Oren, Yael Aylon, editors
MeSH term(s)	Cell Transformation, Neoplastic ; Protein-Serine-Threonine Kinases ; Intracellular Signaling Peptides and Proteins
Language	English
Size	vi, 354 pages :, illustrations
Document type	Book
ISBN	9781461462194 ; 9781461462200 ; 1461462193 ; 1461462207
Database	Catalogue of the US National Library of Medicine (NLM)

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Article ; Online: p53 shades of Hippo.

Furth, Noa / Aylon, Yael / Oren, Moshe

Cell death and differentiation

2017 Volume 25, Issue 1, Page(s) 81–92

Abstract: The three p53 family members, p53, p63 and p73, are structurally similar and share many biochemical activities. Yet, along with their common fundamental role in protecting genomic fidelity, each has acquired distinct functions related to diverse cell ... ...

Abstract	The three p53 family members, p53, p63 and p73, are structurally similar and share many biochemical activities. Yet, along with their common fundamental role in protecting genomic fidelity, each has acquired distinct functions related to diverse cell autonomous and non-autonomous processes. Similar to the p53 family, the Hippo signaling pathway impacts a multitude of cellular processes, spanning from cell cycle and metabolism to development and tumor suppression. The core Hippo module consists of the tumor-suppressive MST-LATS kinases and oncogenic transcriptional co-effectors YAP and TAZ. A wealth of accumulated data suggests a complex and delicate regulatory network connecting the p53 and Hippo pathways, in a highly context-specific manner. This generates multiple layers of interaction, ranging from interdependent and collaborative signaling to apparent antagonistic activity. Furthermore, genetic and epigenetic alterations can disrupt this homeostatic network, paving the way to genomic instability and cancer. This strengthens the need to better understand the nuances that control the molecular function of each component and the cross-talk between the different components. Here, we review interactions between the p53 and Hippo pathways within a subset of physiological contexts, focusing on normal stem cells and development, as well as regulation of apoptosis, senescence and metabolism in transformed cells.
MeSH term(s)	Animals ; Apoptosis ; Carcinogenesis ; Cellular Senescence ; Humans ; Neoplastic Stem Cells/metabolism ; Ploidies ; Protein-Serine-Threonine Kinases/metabolism ; Signal Transduction ; Stem Cells/metabolism ; Transcription Factors/metabolism ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Transcription Factors ; Tumor Suppressor Protein p53 ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2017-10-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/cdd.2017.163
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Article ; Online: p53 deficient breast cancer cells reprogram preadipocytes toward tumor-protective immunomodulatory cells.

Hassin, Ori / Sernik, Miriam / Seligman, Adi / Vogel, Felix C E / Wellenstein, Max D / Smollich, Joachim / Halperin, Coral / Pirona, Anna Chiara / Toledano, Liron Nomi / Caballero, Carolina Dehesa / Schlicker, Lisa / Salame, Tomer-Meir / Sarusi Portuguez, Avital / Aylon, Yael / Scherz-Shouval, Ruth / Geiger, Tamar / de Visser, Karin E / Schulze, Almut / Oren, Moshe

Proceedings of the National Academy of Sciences of the United States of America

2023 Volume 120, Issue 52, Page(s) e2311460120

Abstract: ... ...

Abstract	The
MeSH term(s)	Humans ; Female ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Breast Neoplasms/pathology ; Genes, p53 ; Adipose Tissue/metabolism ; Adipocytes/metabolism ; Tumor Microenvironment/genetics
Chemical Substances	Tumor Suppressor Protein p53
Language	English
Publishing date	2023-12-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2311460120
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