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Article ; Online: Histone demethylase KDM5D upregulation drives sex differences in colon cancer.

2023 Volume 619, Issue 7970, Page(s) 632–639

Abstract: Sex exerts a profound impact on cancer incidence, spectrum and outcomes, yet the molecular and genetic bases of such sex differences are ill-defined and presumptively ascribed to X-chromosome genes and sex ... ...

Abstract	Sex exerts a profound impact on cancer incidence, spectrum and outcomes, yet the molecular and genetic bases of such sex differences are ill-defined and presumptively ascribed to X-chromosome genes and sex hormones
MeSH term(s)	Animals ; Female ; Humans ; Male ; Mice ; CD8-Positive T-Lymphocytes/immunology ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/pathology ; Disease Models, Animal ; Histone Demethylases/genetics ; Histone Demethylases/metabolism ; Mice, Transgenic ; Minor Histocompatibility Antigens/genetics ; Minor Histocompatibility Antigens/metabolism ; Sex Characteristics ; Up-Regulation
Chemical Substances	adenomatous polyposis coli protein, mouse ; APC protein, human ; Histone Demethylases (EC 1.14.11.-) ; KDM5D protein, human (EC 1.14.11.-) ; KRAS protein, human ; Minor Histocompatibility Antigens ; STAT4 protein, human ; Stat4 protein, mouse ; TP53 protein, human ; Trp53 protein, mouse ; Kdm5d protein, mouse (EC 1.14.11.-)
Language	English
Publishing date	2023-06-21
Publishing country	England
Document type	Journal Article
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-023-06254-7
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Article ; Online: Retraction for Braden et al., "Distinct Action of the Retinoblastoma Pathway on the DNA Replication Machinery Defines Specific Roles for Cyclin-Dependent Kinase Complexes in Prereplication Complex Assembly and S-Phase Progression".

Braden, Wesley A / Lenihan, Jon M / Lan, Zhengdao / Luce, K Scott / Zagorski, William / Bosco, Emily / Reed, Michael F / Cook, Jeanette G / Knudsen, Erik S

Molecular and cellular biology

2020 Volume 40, Issue 17

Language	English
Publishing date	2020-08-14
Publishing country	United States
Document type	Journal Article ; Retraction of Publication
ZDB-ID	779397-2
ISSN	1098-5549 ; 0270-7306
ISSN (online)	1098-5549
ISSN	0270-7306
DOI	10.1128/MCB.00319-20
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Zs.A 1666: Show issues

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Article ; Online: Circadian Regulator CLOCK Recruits Immune-Suppressive Microglia into the GBM Tumor Microenvironment.

Chen, Peiwen / Hsu, Wen-Hao / Chang, Andrew / Tan, Zhi / Lan, Zhengdao / Zhou, Ashley / Spring, Denise J / Lang, Frederick F / Wang, Y Alan / DePinho, Ronald A

Cancer discovery

2020 Volume 10, Issue 3, Page(s) 371–381

Abstract: Glioblastoma (GBM) is a lethal brain tumor containing a subpopulation of glioma stem cells (GSC). Pan-cancer analyses have revealed that stemness of cancer cells correlates positively with immunosuppressive pathways in many solid tumors, including GBM, ... ...

Abstract	Glioblastoma (GBM) is a lethal brain tumor containing a subpopulation of glioma stem cells (GSC). Pan-cancer analyses have revealed that stemness of cancer cells correlates positively with immunosuppressive pathways in many solid tumors, including GBM, prompting us to conduct a gain-of-function screen of epigenetic regulators that may influence GSC self-renewal and tumor immunity. The circadian regulator
MeSH term(s)	ARNTL Transcription Factors/genetics ; Animals ; CLOCK Proteins/genetics ; Cell Line, Tumor ; Cell Self Renewal/genetics ; Cell Self Renewal/immunology ; Gene Expression Regulation, Neoplastic/genetics ; Glioblastoma/genetics ; Glioblastoma/immunology ; Glioblastoma/pathology ; Glioblastoma/therapy ; Glycoproteins/genetics ; Heterografts ; Humans ; Immunity, Cellular/immunology ; Mice ; Microglia/immunology ; Microglia/metabolism ; Neoplastic Stem Cells/immunology ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; Tumor Microenvironment/genetics ; Tumor Microenvironment/immunology
Chemical Substances	ARNTL Transcription Factors ; BMAL1 protein, human ; Glycoproteins ; OLFML3 protein, human ; CLOCK Proteins (EC 2.3.1.48) ; CLOCK protein, human (EC 2.3.1.48)
Language	English
Publishing date	2020-01-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-19-0400
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Article ; Online: Symbiotic Macrophage-Glioma Cell Interactions Reveal Synthetic Lethality in PTEN-Null Glioma.

Chen, Peiwen / Zhao, Di / Li, Jun / Liang, Xin / Li, Jiexi / Chang, Andrew / Henry, Verlene K / Lan, Zhengdao / Spring, Denise J / Rao, Ganesh / Wang, Y Alan / DePinho, Ronald A

Cancer cell

2019 Volume 35, Issue 6, Page(s) 868–884.e6

Abstract: Heterotypic interactions across diverse cell types can enable tumor progression and hold the potential to expand therapeutic interventions. Here, combined profiling and functional studies of glioma cells in glioblastoma multiforme (GBM) models establish ... ...

Abstract	Heterotypic interactions across diverse cell types can enable tumor progression and hold the potential to expand therapeutic interventions. Here, combined profiling and functional studies of glioma cells in glioblastoma multiforme (GBM) models establish that PTEN deficiency activates YAP1, which directly upregulates lysyl oxidase (LOX) expression. Mechanistically, secreted LOX functions as a potent macrophage chemoattractant via activation of the β1 integrin-PYK2 pathway in macrophages. These infiltrating macrophages secrete SPP1, which sustains glioma cell survival and stimulates angiogenesis. In PTEN-null GBM models, LOX inhibition markedly suppresses macrophage infiltration and tumor progression. Correspondingly, YAP1-LOX and β1 integrin-SPP1 signaling correlates positively with higher macrophage density and lower overall survival in GBM patients. This symbiotic glioma-macrophage interplay provides therapeutic targets specifically for PTEN-deficient GBM.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Antineoplastic Agents/pharmacology ; Biomarkers, Tumor/deficiency ; Biomarkers, Tumor/genetics ; Brain Neoplasms/drug therapy ; Brain Neoplasms/enzymology ; Brain Neoplasms/genetics ; Brain Neoplasms/pathology ; Cell Movement ; Cell Proliferation ; Enzyme Inhibitors/pharmacology ; Female ; Focal Adhesion Kinase 2/genetics ; Focal Adhesion Kinase 2/metabolism ; Gene Expression Regulation, Neoplastic ; Glioma/drug therapy ; Glioma/enzymology ; Glioma/genetics ; Glioma/pathology ; HEK293 Cells ; Humans ; Integrin beta1/genetics ; Integrin beta1/metabolism ; Macrophages/drug effects ; Macrophages/enzymology ; Macrophages/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred ICR ; Mice, SCID ; Osteopontin/genetics ; Osteopontin/metabolism ; PTEN Phosphohydrolase/deficiency ; PTEN Phosphohydrolase/genetics ; Paracrine Communication/drug effects ; Protein-Lysine 6-Oxidase/antagonists & inhibitors ; Protein-Lysine 6-Oxidase/genetics ; Protein-Lysine 6-Oxidase/metabolism ; RAW 264.7 Cells ; Signal Transduction ; Synthetic Lethal Mutations ; THP-1 Cells ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Tumor Burden ; Xenograft Model Antitumor Assays ; YAP-Signaling Proteins
Chemical Substances	Adaptor Proteins, Signal Transducing ; Antineoplastic Agents ; Biomarkers, Tumor ; Enzyme Inhibitors ; Integrin beta1 ; SPP1 protein, human ; Transcription Factors ; YAP-Signaling Proteins ; YAP1 protein, human ; Osteopontin (106441-73-0) ; LOX protein, human (EC 1.4.3.13) ; Protein-Lysine 6-Oxidase (EC 1.4.3.13) ; Focal Adhesion Kinase 2 (EC 2.7.10.2) ; PTK2B protein, human (EC 2.7.10.2) ; PTEN Phosphohydrolase (EC 3.1.3.67) ; PTEN protein, human (EC 3.1.3.67)
Language	English
Publishing date	2019-06-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2019.05.003
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Article ; Online: Tumor Microenvironment Remodeling Enables Bypass of Oncogenic KRAS Dependency in Pancreatic Cancer.

Hou, Pingping / Kapoor, Avnish / Zhang, Qiang / Li, Jiexi / Wu, Chang-Jiun / Li, Jun / Lan, Zhengdao / Tang, Ming / Ma, Xingdi / Ackroyd, Jeffrey J / Kalluri, Raghu / Zhang, Jianhua / Jiang, Shan / Spring, Denise J / Wang, Y Alan / DePinho, Ronald A

Cancer discovery

2020 Volume 10, Issue 7, Page(s) 1058–1077

Abstract: Oncogenic KRAS (KRAS*) is a key tumor maintenance gene in pancreatic ductal adenocarcinoma (PDAC), motivating pharmacologic targeting of KRAS* and its effectors. Here, we explored mechanisms involving the tumor microenvironment (TME) as a potential basis ...

Abstract	Oncogenic KRAS (KRAS) is a key tumor maintenance gene in pancreatic ductal adenocarcinoma (PDAC), motivating pharmacologic targeting of KRAS and its effectors. Here, we explored mechanisms involving the tumor microenvironment (TME) as a potential basis for resistance to targeting KRAS*. Using the inducible
MeSH term(s)	Humans ; Oncogenes/physiology ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; Proto-Oncogene Proteins p21(ras)/metabolism ; Tumor Microenvironment ; Pancreatic Neoplasms
Chemical Substances	KRAS protein, human ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2020-04-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-19-0597
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Zs.A 6916: Show issues

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Article ; Online: P4HA2-induced prolyl hydroxylation suppresses YAP1-mediated prostate cancer cell migration, invasion, and metastasis.

Oncogene

2021 Volume 40, Issue 41, Page(s) 6049–6056

Abstract: Yes-associated protein 1 (YAP1), a key player in the Hippo pathway, has been shown to play a critical role in tumor progression. However, the role of YAP1 in prostate cancer cell invasion, migration, and metastasis is not well defined. Through functional, ...

Abstract	Yes-associated protein 1 (YAP1), a key player in the Hippo pathway, has been shown to play a critical role in tumor progression. However, the role of YAP1 in prostate cancer cell invasion, migration, and metastasis is not well defined. Through functional, transcriptomic, epigenomic, and proteomic analyses, we showed that prolyl hydroxylation of YAP1 plays a critical role in the suppression of cell migration, invasion, and metastasis in prostate cancer. Knockdown (KD) or knockout (KO) of YAP1 led to an increase in cell migration, invasion, and metastasis in prostate cancer cells. Microarray analysis showed that the EMT pathway was activated in Yap1-KD cells. ChIP-seq analysis showed that YAP1 target genes are enriched in pathways regulating cell migration. Mass spectrometry analysis identified P4H prolyl hydroxylase in the YAP1 complex and YAP1 was hydroxylated at multiple proline residues. Proline-to-alanine mutations of YAP1 isoform 3 identified proline 174 as a critical residue, and its hydroxylation suppressed cell migration, invasion, and metastasis. KO of P4ha2 led to an increase in cell migration and invasion, which was reversed upon Yap1 KD. Our study identified a novel regulatory mechanism of YAP1 by which P4HA2-dependent prolyl hydroxylation of YAP1 determines its transcriptional activities and its function in prostate cancer metastasis.
MeSH term(s)	Animals ; Cell Movement/physiology ; Humans ; Male ; Mice ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Prolyl Hydroxylases/metabolism ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; YAP-Signaling Proteins/antagonists & inhibitors ; YAP-Signaling Proteins/metabolism
Chemical Substances	YAP-Signaling Proteins ; Yap1 protein, mouse ; P4HA2 protein, human (EC 1.14.11.-) ; Prolyl Hydroxylases (EC 1.14.11.-)
Language	English
Publishing date	2021-09-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-021-02000-3
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Zs.A 2218: Show issues

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Article ; Online: Chromatin Regulator CHD1 Remodels the Immunosuppressive Tumor Microenvironment in PTEN-Deficient Prostate Cancer.

Cancer discovery

2020 Volume 10, Issue 9, Page(s) 1374–1387

Abstract: Genetic inactivation ... ...

Abstract	Genetic inactivation of
MeSH term(s)	Animals ; Cell Line, Tumor ; DNA-Binding Proteins/metabolism ; Disease Models, Animal ; Gene Expression Regulation, Neoplastic/immunology ; Humans ; Male ; Mice, Transgenic ; PTEN Phosphohydrolase/genetics ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/immunology ; Prostatic Neoplasms/pathology ; Smad4 Protein/genetics ; Tumor Escape/genetics ; Tumor Microenvironment/genetics ; Tumor Microenvironment/immunology
Chemical Substances	Chd1 protein, mouse ; DNA-Binding Proteins ; Smad4 Protein ; Smad4 protein, mouse ; PTEN Phosphohydrolase (EC 3.1.3.67) ; Pten protein, mouse (EC 3.1.3.67)
Language	English
Publishing date	2020-05-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-19-1352
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Zs.A 6916: Show issues

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Article ; Online: Telomere dysfunction activates YAP1 to drive tissue inflammation.

Chakravarti, Deepavali / Hu, Baoli / Mao, Xizeng / Rashid, Asif / Li, Jiexi / Li, Jun / Liao, Wen-Ting / Whitley, Elizabeth M / Dey, Prasenjit / Hou, Pingping / LaBella, Kyle A / Chang, Andrew / Wang, Guocan / Spring, Denise J / Deng, Pingna / Zhao, Di / Liang, Xin / Lan, Zhengdao / Lin, Yiyun /

Sarkar, Sharmistha / Terranova, Christopher / Deribe, Yonathan Lissanu / Blutt, Sarah E / Okhuysen, Pablo / Zhang, Jianhua / Vilar, Eduardo / Nielsen, Ole Haagen / Dupont, Andrew / Younes, Mamoun / Patel, Kalyani R / Shroyer, Noah F / Rai, Kunal / Estes, Mary K / Wang, Y Alan / Bertuch, Alison A / DePinho, Ronald A

Nature communications

2020 Volume 11, Issue 1, Page(s) 4766

Abstract: Germline telomere maintenance defects are associated with an increased incidence of inflammatory diseases in humans, yet whether and how telomere dysfunction causes inflammation are not known. Here, we show that telomere dysfunction drives pATM/c-ABL- ... ...

Abstract	Germline telomere maintenance defects are associated with an increased incidence of inflammatory diseases in humans, yet whether and how telomere dysfunction causes inflammation are not known. Here, we show that telomere dysfunction drives pATM/c-ABL-mediated activation of the YAP1 transcription factor, up-regulating the major pro-inflammatory factor, pro-IL-18. The colonic microbiome stimulates cytosolic receptors activating caspase-1 which cleaves pro-IL-18 into mature IL-18, leading to recruitment of interferon (IFN)-γ-secreting T cells and intestinal inflammation. Correspondingly, patients with germline telomere maintenance defects exhibit DNA damage (γH2AX) signaling together with elevated YAP1 and IL-18 expression. In mice with telomere dysfunction, telomerase reactivation in the intestinal epithelium or pharmacological inhibition of ATM, YAP1, or caspase-1 as well as antibiotic treatment, dramatically reduces IL-18 and intestinal inflammation. Thus, telomere dysfunction-induced activation of the ATM-YAP1-pro-IL-18 pathway in epithelium is a key instigator of tissue inflammation.
MeSH term(s)	Adaptor Proteins, Signal Transducing/antagonists & inhibitors ; Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Anti-Bacterial Agents/therapeutic use ; Ataxia Telangiectasia Mutated Proteins/antagonists & inhibitors ; Ataxia Telangiectasia Mutated Proteins/metabolism ; Caspase 1/metabolism ; Cell Cycle Proteins/antagonists & inhibitors ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Child ; Colon/metabolism ; Colon/microbiology ; Colon/pathology ; Gastrointestinal Diseases/pathology ; Gastrointestinal Microbiome/drug effects ; Gastrointestinal Microbiome/physiology ; Humans ; Inflammation/drug therapy ; Inflammation/metabolism ; Inflammation/microbiology ; Inflammation/pathology ; Interleukin-18/genetics ; Interleukin-18/metabolism ; Intestinal Mucosa/metabolism ; Intestinal Mucosa/pathology ; Mice ; Mice, Mutant Strains ; Phosphorylation ; Protein Precursors/genetics ; Protein Precursors/metabolism ; Signal Transduction ; Telomerase/genetics ; Telomerase/metabolism ; Telomere/pathology ; YAP-Signaling Proteins
Chemical Substances	Adaptor Proteins, Signal Transducing ; Anti-Bacterial Agents ; Cell Cycle Proteins ; Interleukin-18 ; Protein Precursors ; YAP-Signaling Proteins ; Yap1 protein, mouse ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; Atm protein, mouse (EC 2.7.11.1) ; Telomerase (EC 2.7.7.49) ; Tert protein, mouse (EC 2.7.7.49) ; Casp1 protein, mouse (EC 3.4.22.36) ; Caspase 1 (EC 3.4.22.36)
Language	English
Publishing date	2020-09-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-020-18420-w
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: KRAS-IRF2 Axis Drives Immune Suppression and Immune Therapy Resistance in Colorectal Cancer.

Liao, Wenting / Overman, Michael J / Boutin, Adam T / Shang, Xiaoying / Zhao, Di / Dey, Prasenjit / Li, Jiexi / Wang, Guocan / Lan, Zhengdao / Li, Jun / Tang, Ming / Jiang, Shan / Ma, Xingdi / Chen, Peiwen / Katkhuda, Riham / Korphaisarn, Krittiya / Chakravarti, Deepavali / Chang, Andrew / Spring, Denise J /

Chang, Qing / Zhang, Jianhua / Maru, Dipen M / Maeda, Dean Y / Zebala, John A / Kopetz, Scott / Wang, Y Alan / DePinho, Ronald A

Cancer cell

2019 Volume 35, Issue 4, Page(s) 559–572.e7

Abstract: The biological functions and mechanisms of oncogenic ... ...

Abstract	The biological functions and mechanisms of oncogenic KRAS
MeSH term(s)	Adenomatous Polyposis Coli Protein/genetics ; Adenomatous Polyposis Coli Protein/metabolism ; Adult ; Aged ; Animals ; Antineoplastic Agents, Immunological/pharmacology ; Cell Line, Tumor ; Cell Movement ; Chemokines, CXC/metabolism ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/immunology ; Colorectal Neoplasms/metabolism ; Drug Resistance, Neoplasm/genetics ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Interferon Regulatory Factor-2/genetics ; Interferon Regulatory Factor-2/metabolism ; Male ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; Middle Aged ; Myeloid-Derived Suppressor Cells/drug effects ; Myeloid-Derived Suppressor Cells/immunology ; Myeloid-Derived Suppressor Cells/metabolism ; Programmed Cell Death 1 Receptor/antagonists & inhibitors ; Programmed Cell Death 1 Receptor/immunology ; Programmed Cell Death 1 Receptor/metabolism ; Proto-Oncogene Proteins p21(ras)/genetics ; Proto-Oncogene Proteins p21(ras)/metabolism ; Receptors, Interleukin-8B/metabolism ; Signal Transduction ; Tumor Escape ; Tumor Microenvironment ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Young Adult
Chemical Substances	Adenomatous Polyposis Coli Protein ; Antineoplastic Agents, Immunological ; Chemokines, CXC ; Cxcl3 protein, mouse ; Interferon Regulatory Factor-2 ; Irf2 protein, mouse ; Pdcd1 protein, mouse ; Programmed Cell Death 1 Receptor ; Receptors, Interleukin-8B ; Trp53 protein, mouse ; Tumor Suppressor Protein p53 ; adenomatous polyposis coli protein, mouse ; Hras protein, mouse (EC 3.6.5.2) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2019-03-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2019.02.008
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Zs.MG 104: Show issues

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Article ; Online: Synthetic essentiality of chromatin remodelling factor CHD1 in PTEN-deficient cancer.

Nature

2017 Volume 542, Issue 7642, Page(s) 484–488

Abstract: Synthetic lethality and collateral lethality are two well-validated conceptual strategies for identifying therapeutic targets in cancers with tumour-suppressor gene deletions. Here, we explore an approach to identify potential synthetic-lethal ... ...

Abstract	Synthetic lethality and collateral lethality are two well-validated conceptual strategies for identifying therapeutic targets in cancers with tumour-suppressor gene deletions. Here, we explore an approach to identify potential synthetic-lethal interactions by screening mutually exclusive deletion patterns in cancer genomes. We sought to identify 'synthetic-essential' genes: those that are occasionally deleted in some cancers but are almost always retained in the context of a specific tumour-suppressor deficiency. We also posited that such synthetic-essential genes would be therapeutic targets in cancers that harbour specific tumour-suppressor deficiencies. In addition to known synthetic-lethal interactions, this approach uncovered the chromatin helicase DNA-binding factor CHD1 as a putative synthetic-essential gene in PTEN-deficient cancers. In PTEN-deficient prostate and breast cancers, CHD1 depletion profoundly and specifically suppressed cell proliferation, cell survival and tumorigenic potential. Mechanistically, functional PTEN stimulates the GSK3β-mediated phosphorylation of CHD1 degron domains, which promotes CHD1 degradation via the β-TrCP-mediated ubiquitination-proteasome pathway. Conversely, PTEN deficiency results in stabilization of CHD1, which in turn engages the trimethyl lysine-4 histone H3 modification to activate transcription of the pro-tumorigenic TNF-NF-κB gene network. This study identifies a novel PTEN pathway in cancer and provides a framework for the discovery of 'trackable' targets in cancers that harbour specific tumour-suppressor deficiencies.
MeSH term(s)	Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Chromatin Assembly and Disassembly/genetics ; DNA Helicases/chemistry ; DNA Helicases/deficiency ; DNA Helicases/genetics ; DNA Helicases/metabolism ; DNA-Binding Proteins/chemistry ; DNA-Binding Proteins/deficiency ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Genes, Essential/genetics ; Glycogen Synthase Kinase 3 beta/metabolism ; Histones/metabolism ; Humans ; Lysine/metabolism ; Male ; Methylation ; Molecular Targeted Therapy ; NF-kappa B/metabolism ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; PTEN Phosphohydrolase/deficiency ; PTEN Phosphohydrolase/genetics ; PTEN Phosphohydrolase/metabolism ; Phosphorylation ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Proteasome Endopeptidase Complex/metabolism ; Protein Stability ; Proteolysis ; Tumor Necrosis Factor-alpha/metabolism ; Ubiquitination ; beta-Transducin Repeat-Containing Proteins/metabolism
Chemical Substances	BTRC protein, human ; DNA-Binding Proteins ; Histones ; NF-kappa B ; Tumor Necrosis Factor-alpha ; beta-Transducin Repeat-Containing Proteins ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; PTEN Phosphohydrolase (EC 3.1.3.67) ; PTEN protein, human (EC 3.1.3.67) ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; DNA Helicases (EC 3.6.4.-) ; CHD1 protein, human (EC 3.6.4.12) ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2017-02-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/nature21357
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 26: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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