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Article ; Online: Multi-omics investigation reveals functional specialization of transcriptional cyclin dependent kinases in cancer biology.

Donovan, Micah G / Galbraith, Matthew D / Espinosa, Joaquin M

2022 Volume 12, Issue 1, Page(s) 22505

Abstract: Transcriptional addiction is recognized as a valid therapeutic target in cancer, whereby the dependency of cancer cells on oncogenic transcriptional regulators may be pharmacologically exploited. However, a comprehensive understanding of the key factors ... ...

Abstract	Transcriptional addiction is recognized as a valid therapeutic target in cancer, whereby the dependency of cancer cells on oncogenic transcriptional regulators may be pharmacologically exploited. However, a comprehensive understanding of the key factors within the transcriptional machinery that might afford a useful therapeutic window remains elusive. Herein, we present a cross-omics investigation into the functional specialization of the transcriptional cyclin dependent kinases (tCDKs) through analysis of high-content genetic dependency, gene expression, patient survival, and drug response datasets. This analysis revealed specialization among tCDKs in terms of contributions to cancer cell fitness, clinical prognosis, and interaction with oncogenic signaling pathways. CDK7 and CDK9 stand out as the most relevant targets, albeit through distinct mechanisms of oncogenicity and context-dependent contributions to cancer survival and drug sensitivity. Genetic ablation of CDK9, but not CDK7, mimics the effect on cell viability the loss of key components of the transcriptional machinery. Pathway analysis of genetic co-dependency and drug sensitivity data show CDK7 and CDK9 have distinct relationships with major oncogenic signatures, including MYC and E2F targets, oxidative phosphorylation, and the unfolded protein response. Altogether, these results inform the improved design of therapeutic strategies targeting tCDKs in cancer.
MeSH term(s)	Humans ; Cyclin-Dependent Kinases/genetics ; Cyclin-Dependent Kinases/metabolism ; Multiomics ; Signal Transduction ; Neoplasms/genetics ; Cyclins/metabolism
Chemical Substances	Cyclin-Dependent Kinases (EC 2.7.11.22) ; Cyclins
Language	English
Publishing date	2022-12-28
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-26860-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Global Analyses to Identify Direct Transcriptional Targets of p53.

Galbraith, Matthew D / Andrysik, Zdenek / Sullivan, Kelly D / Espinosa, Joaquín M

Methods in molecular biology (Clifton, N.J.)

2021 Volume 2267, Page(s) 19–56

Abstract: The transcription factor p53 controls a gene expression program with pleiotropic effects on cell biology including cell cycle arrest and apoptosis. Identifying direct p53 target genes within this network and determining how they influence cell fate ... ...

Abstract	The transcription factor p53 controls a gene expression program with pleiotropic effects on cell biology including cell cycle arrest and apoptosis. Identifying direct p53 target genes within this network and determining how they influence cell fate decisions downstream of p53 activation is a prerequisite for designing therapeutic approaches that target p53 to effectively kill cancer cells. Here we describe a comprehensive multi-omics approach for identifying genes that are direct transcriptional targets of p53. We provide detailed procedures for measuring global RNA polymerase activity, defining p53 binding sites across the genome, and quantifying changes in steady-state mRNA in response to p53 activation.
MeSH term(s)	Animals ; Cell Line ; Chromatin Immunoprecipitation Sequencing/methods ; Genomics/methods ; Humans ; RNA-Seq/methods ; Transcriptional Activation ; Transcriptome ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Tumor Suppressor Protein p53
Language	English
Publishing date	2021-03-31
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.
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-1217-0_3
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Article ; Online: Multi-omics analysis reveals contextual tumor suppressive and oncogenic gene modules within the acute hypoxic response.

Andrysik, Zdenek / Bender, Heather / Galbraith, Matthew D / Espinosa, Joaquin M

Nature communications

2021 Volume 12, Issue 1, Page(s) 1375

Abstract: Cellular adaptation to hypoxia is a hallmark of cancer, but the relative contribution of hypoxia-inducible factors (HIFs) versus other oxygen sensors to tumorigenesis is unclear. We employ a multi-omics pipeline including measurements of nascent RNA to ... ...

Abstract	Cellular adaptation to hypoxia is a hallmark of cancer, but the relative contribution of hypoxia-inducible factors (HIFs) versus other oxygen sensors to tumorigenesis is unclear. We employ a multi-omics pipeline including measurements of nascent RNA to characterize transcriptional changes upon acute hypoxia. We identify an immediate early transcriptional response that is strongly dependent on HIF1A and the kinase activity of its cofactor CDK8, includes indirect repression of MYC targets, and is highly conserved across cancer types. HIF1A drives this acute response via conserved high-occupancy enhancers. Genetic screen data indicates that, in normoxia, HIF1A displays strong cell-autonomous tumor suppressive effects through a gene module mediating mTOR inhibition. Conversely, in advanced malignancies, expression of a module of HIF1A targets involved in collagen remodeling is associated with poor prognosis across diverse cancer types. In this work, we provide a valuable resource for investigating context-dependent roles of HIF1A and its targets in cancer biology.
MeSH term(s)	Cell Line, Tumor ; Cell Survival ; Cyclin-Dependent Kinase 8/metabolism ; Disease Progression ; Gene Expression Regulation, Neoplastic ; Gene Regulatory Networks ; Genes, Tumor Suppressor ; Genome, Human ; Genomics ; Humans ; Hypoxia/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Neoplasms/genetics ; Neoplasms/pathology ; Oncogenes ; Protein Binding ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; TOR Serine-Threonine Kinases/metabolism ; Transcription, Genetic ; Transcriptional Activation/genetics ; Up-Regulation/genetics
Chemical Substances	Hypoxia-Inducible Factor 1, alpha Subunit ; RNA, Messenger ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; CDK8 protein, human (EC 2.7.11.22) ; Cyclin-Dependent Kinase 8 (EC 2.7.11.22)
Language	English
Publishing date	2021-03-02
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/s41467-021-21687-2
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Article ; Online: Multi-omics analysis reveals contextual tumor suppressive and oncogenic gene modules within the acute hypoxic response

Zdenek Andrysik / Heather Bender / Matthew D. Galbraith / Joaquin M. Espinosa

Nature Communications, Vol 12, Iss 1, Pp 1-

2021 Volume 18

Abstract: The response to hypoxia can significantly impact oncogenic processes. Here, the authors define the early transcriptional response to acute hypoxia and identify HIF1A target genes as part of this acute response, providing a resource for investigating ... ...

Abstract	The response to hypoxia can significantly impact oncogenic processes. Here, the authors define the early transcriptional response to acute hypoxia and identify HIF1A target genes as part of this acute response, providing a resource for investigating context-dependent roles of HIF1A in the biology of cancer.
Keywords	Science ; Q
Language	English
Publishing date	2021-03-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: In vivo

D'Alessandro, Angelo / Nouraie, S Mehdi / Zhang, Yingze / Cendali, Francesca / Gamboni, Fabia / Reisz, Julie A / Zhang, Xu / Bartsch, Kyle W / Galbraith, Matthew D / Gordeuk, Victor R / Gladwin, Mark T

bioRxiv : the preprint server for biology

2023

Abstract: Despite a wealth of exploratory plasma metabolomics studies in sickle cell disease (SCD), no study to date has evaluate a large and well phenotyped cohort to compare the primary erythrocyte metabolome of hemoglobin SS, SC and transfused AA red blood ... ...

Abstract	Despite a wealth of exploratory plasma metabolomics studies in sickle cell disease (SCD), no study to date has evaluate a large and well phenotyped cohort to compare the primary erythrocyte metabolome of hemoglobin SS, SC and transfused AA red blood cells (RBCs) Key points: In vivo dysregulation of RBC metabolism by HbS is evaluated by metabolic profiling of 587 patients with variable HbA, HbC and HbF levels;RBC acyl-carnitines, urate, pyruvate metabolism, S1P, kynurenine relate to hemolysis and cardiorenal dysfunction, respond to transfusion.
Language	English
Publishing date	2023-02-14
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.02.13.528368
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Article: Metabolic signatures of cardiorenal dysfunction in plasma from sickle cell patients, as a function of therapeutic transfusion and hydroxyurea treatment.

D'Alessandro, Angelo / Nouraie, S Mehdi / Zhang, Yingze / Cendali, Francesca / Gamboni, Fabia / Reisz, Julie A / Zhang, Xu / Bartsch, Kyle W / Galbraith, Matthew D / Espinosa, Joaquin M / Gordeuk, Victor R / Gladwin, Mark T

bioRxiv : the preprint server for biology

2023

Abstract: Metabolomics studies in sickle cell disease (SCD) have been so far limited to tens of samples, owing to technical and experimental limitations. To overcome these limitations, we performed plasma metabolomics analyses on 596 samples from patients with ... ...

Abstract	Metabolomics studies in sickle cell disease (SCD) have been so far limited to tens of samples, owing to technical and experimental limitations. To overcome these limitations, we performed plasma metabolomics analyses on 596 samples from patients with sickle cell sickle cell disease (SCD) enrolled in the WALK-PHaSST study. Clinical covariates informed the biological interpretation of metabolomics data, including genotypes (hemoglobin SS, hemoglobin SC), history of recent transfusion (HbA%), response to hydroxyurea treatment (HbF%). We investigated metabolic correlates to the degree of hemolysis, cardiorenal function, as determined by tricuspid regurgitation velocity (TRV), estimated glomerular filtration rate (eGFR), and overall hazard ratio (unadjusted or adjusted by age). Recent transfusion events or hydroxyurea treatment were associated with elevation in plasma free fatty acids and decreases in acyl-carnitines, urate, kynurenine, indoles, carboxylic acids, and glycine- or taurine-conjugated bile acids. High levels of these metabolites, along with low levels of plasma S1P and L-arginine were identified as top markers of hemolysis, cardiorenal function (TRV, eGFR), and overall hazard ratio. We thus uploaded all omics and clinical data on a novel online portal that we used to identify a potential mechanism of dysregulated red cell S1P synthesis and export as a contributor to the more severe clinical manifestations in patients with the SS genotype compared to SC. In conclusion, plasma metabolic signatures - including low S1P, arginine and elevated kynurenine, acyl-carnitines and bile acids - are associated with clinical manifestation and therapeutic efficacy in SCD patients, suggesting new avenues for metabolic interventions in this patient population.
Language	English
Publishing date	2023-04-06
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.04.05.535693
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Article ; Online: In vivo evaluation of the effect of sickle cell hemoglobin S, C and therapeutic transfusion on erythrocyte metabolism and cardiorenal dysfunction.

American journal of hematology

2023 Volume 98, Issue 7, Page(s) 1017–1028

Abstract	Despite a wealth of exploratory plasma metabolomics studies in sickle cell disease (SCD), no study to date has evaluate a large and well phenotyped cohort to compare the primary erythrocyte metabolome of hemoglobin SS, SC and transfused AA red blood cells (RBCs) in vivo. The current study evaluates the RBC metabolome of 587 subjects with sickle cell sickle cell disease (SCD) from the WALK-PHaSST clinical cohort. The set includes hemoglobin SS, hemoglobin SC SCD patients, with variable levels of HbA related to RBC transfusion events. Here we explore the modulating effects of genotype, age, sex, severity of hemolysis, and transfusion therapy on sickle RBC metabolism. Results show that RBCs from patients with Hb SS genotypes-compared to AA RBCs from recent transfusion events or SC RBCs-are characterized by significant alterations of RBC acylcarnitines, pyruvate, sphingosine 1-phosphate, creatinine, kynurenine and urate metabolism. Surprisingly, the RBC metabolism of SC RBCs is dramatically different from SS, with all glycolytic intermediates significantly elevated in SS RBCs, with the exception of pyruvate. This result suggests a metabolic blockade at the ATP-generating phosphoenolpyruvate to pyruvate step of glycolysis, which is catalyzed by redox-sensitive pyruvate kinase. Metabolomics, clinical and hematological data were collated in a novel online portal. In conclusion, we identified metabolic signatures of HbS RBCs that correlate with the degree of steady state hemolytic anemia, cardiovascular and renal dysfunction and mortality.
MeSH term(s)	Humans ; Hemoglobin, Sickle/metabolism ; Erythrocytes/metabolism ; Anemia, Sickle Cell ; Sickle Cell Trait ; Pyruvates/metabolism
Chemical Substances	Hemoglobin, Sickle ; Pyruvates
Language	English
Publishing date	2023-04-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	196767-8
ISSN	1096-8652 ; 0361-8609
ISSN (online)	1096-8652
ISSN	0361-8609
DOI	10.1002/ajh.26923
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Article: Mediator kinase inhibition suppresses hyperactive interferon signaling in Down syndrome.

Cozzolino, Kira / Sanford, Lynn / Hunter, Samuel / Molison, Kayla / Erickson, Benjamin / Jones, Taylor / Ajit, Deepa / Galbraith, Matthew D / Espinosa, Joaquin M / Bentley, David L / Allen, Mary A / Dowell, Robin D / Taatjes, Dylan J

bioRxiv : the preprint server for biology

2023

Abstract: Hyperactive interferon (IFN) signaling is a hallmark of Down syndrome (DS), a condition caused by trisomy 21 (T21); strategies that normalize IFN signaling could benefit this population. Mediator-associated kinases CDK8 and CDK19 drive inflammatory ... ...

Abstract	Hyperactive interferon (IFN) signaling is a hallmark of Down syndrome (DS), a condition caused by trisomy 21 (T21); strategies that normalize IFN signaling could benefit this population. Mediator-associated kinases CDK8 and CDK19 drive inflammatory responses through incompletely understood mechanisms. Using sibling-matched cell lines with/without T21, we investigated Mediator kinase function in the context of hyperactive IFN in DS. Activation of IFN-response genes was suppressed in cells treated with the CDK8/CDK19 inhibitor cortistatin A, and this occurred through suppression of IFN-responsive transcription factor activity. Moreover, we discovered that CDK8/CDK19 affect splicing, a novel means by which Mediator kinases control gene expression. Kinase inhibition altered splicing in pathway-specific ways and selectively affected IFN-responsive gene splicing in T21 cells. To further probe Mediator kinase function, we completed cytokine screens and untargeted metabolomics experiments. Cytokines are master regulators of inflammatory responses; by screening 105 different cytokine proteins, we show that Mediator kinases help drive IFN-dependent cytokine responses at least in part through transcriptional regulation of cytokine genes and receptors. Metabolomics revealed that Mediator kinase inhibition altered core metabolic pathways, including broad up-regulation of anti-inflammatory lipid mediators. Elevated levels of lipid mediators persisted at least 24hr after Mediator kinase inhibition, and many identified lipids serve as ligands for nuclear receptors (e.g. PPAR, LXR) or G-protein coupled receptors (GPCRs; e.g. FFAR4). Notably, ligand-dependent activation of these GPCRs or nuclear receptors will propagate anti-inflammatory signaling pathways and gene expression programs, and this mechanistic link suggests that metabolic changes caused by CDK8/CDK19 inhibition can durably and independently suppress pro-inflammatory IFN responses. Collectively, our results establish that Mediator kinase inhibition antagonizes IFN signaling through transcriptional, metabolic, and cytokine responses, with implications for DS and other chronic inflammatory conditions.
Language	English
Publishing date	2023-12-13
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.07.05.547813
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Article ; Online: FAM193A is a positive regulator of p53 activity.

Szwarc, Maria M / Guarnieri, Anna L / Joshi, Molishree / Duc, Huy N / Laird, Madison C / Pandey, Ahwan / Khanal, Santosh / Dohm, Emily / Bui, Aimee K / Sullivan, Kelly D / Galbraith, Matthew D / Andrysik, Zdenek / Espinosa, Joaquin M

Cell reports

2023 Volume 42, Issue 3, Page(s) 112230

Abstract: Inactivation of the p53 tumor suppressor, either by mutations or through hyperactivation of repressors such as MDM2 and MDM4, is a hallmark of cancer. Although many inhibitors of the p53-MDM2/4 interaction have been developed, such as Nutlin, their ... ...

Abstract	Inactivation of the p53 tumor suppressor, either by mutations or through hyperactivation of repressors such as MDM2 and MDM4, is a hallmark of cancer. Although many inhibitors of the p53-MDM2/4 interaction have been developed, such as Nutlin, their therapeutic value is limited by highly heterogeneous cellular responses. We report here a multi-omics investigation of the cellular response to MDM2/4 inhibitors, leading to identification of FAM193A as a widespread regulator of p53 function. CRISPR screening identified FAM193A as necessary for the response to Nutlin. FAM193A expression correlates with Nutlin sensitivity across hundreds of cell lines. Furthermore, genetic codependency data highlight FAM193A as a component of the p53 pathway across diverse tumor types. Mechanistically, FAM193A interacts with MDM4, and FAM193A depletion stabilizes MDM4 and inhibits the p53 transcriptional program. Last, FAM193A expression is associated with better prognosis in multiple malignancies. Altogether, these results identify FAM193A as a positive regulator of p53.
MeSH term(s)	Humans ; Antineoplastic Agents/pharmacology ; Apoptosis ; Cell Cycle Proteins/metabolism ; Cell Line, Tumor ; Neoplasms/pathology ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-mdm2/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Antineoplastic Agents ; Cell Cycle Proteins ; MDM4 protein, human ; Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-mdm2 (EC 2.3.2.27) ; Tumor Suppressor Protein p53 ; FAM193A protein, human
Language	English
Publishing date	2023-03-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.112230
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Article ; Online: Metabolic signatures of cardiorenal dysfunction in plasma from sickle cell patients as a function of therapeutic transfusion and hydroxyurea treatment.

Haematologica

2023 Volume 108, Issue 12, Page(s) 3418–3432

Abstract	Metabolomics studies in sickle cell disease (SCD) have been so far limited to tens of samples, owing to technical and experimental limitations. To overcome these limitations, we performed plasma metabolomics analyses on 596 samples from patients with SCD enrolled in the WALK-PHaSST study (clinicaltrials gov. Identifier: NCT00492531). Clinical covariates informed the biological interpretation of metabolomics data, including genotypes (hemoglobin [Hb] SS, hemoglobin SC), history of recent transfusion (HbA%), response to hydroxyurea treatment (fetal Hb%). We investigated metabolic correlates to the degree of intravascular hemolysis, cardiorenal function, as determined by tricuspid regurgitation velocity (TRV), estimated glomerular filtration rate (eGFR), and overall hazard ratio (unadjusted or adjusted by age). Recent transfusion events or hydroxyurea treatment were associated with elevation in plasma-free fatty acids and decreases in acyl-carnitines, urate, kynurenine, indoles, carboxylic acids, and glycine- or taurine-conjugated bile acids. High levels of these metabolites, along with low levels of plasma S1P and L-arginine were identified as top markers of hemolysis, cardiorenal function (TRV, eGFR), and overall hazard ratio. We thus uploaded all omics and clinical data on a novel online portal that we used to identify a potential mechanism of dysregulated red cell S1P synthesis and export as a contributor to the more severe clinical manifestations in patients with the SS genotype compared to SC. In conclusion, plasma metabolic signatures - including low S1P, arginine and elevated kynurenine, acyl-carnitines and bile acids - are associated with clinical manifestation and therapeutic efficacy in SCD patients, suggesting new avenues for metabolic interventions in this patient population.
MeSH term(s)	Humans ; Hydroxyurea/therapeutic use ; Kynurenine/therapeutic use ; Anemia, Sickle Cell/complications ; Anemia, Sickle Cell/drug therapy ; Hemoglobin SC Disease/complications ; Hemolysis ; Hemoglobin, Sickle ; Bile Acids and Salts/therapeutic use
Chemical Substances	Hydroxyurea (X6Q56QN5QC) ; Kynurenine (343-65-7) ; Hemoglobin, Sickle ; Bile Acids and Salts
Language	English
Publishing date	2023-12-01
Publishing country	Italy
Document type	Journal Article
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2023.283288
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