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Article ; Online: SLC25A32 sustains cancer cell proliferation by regulating flavin adenine nucleotide (FAD) metabolism.

Santoro, Valeria / Kovalenko, Ilya / Vriens, Kim / Christen, Stefan / Bernthaler, Andreas / Haegebarth, Andrea / Fendt, Sarah-Maria / Christian, Sven

Oncotarget

2020 Volume 11, Issue 8, Page(s) 801–812

Abstract: SLC25A32 is a member of the solute carrier 25 family of mitochondrial transporters. SLC25A32 transports tetrahydrofolate (THF) as well as FAD into mitochondria and regulates mitochondrial one-carbon metabolism and redox balance. While it is known that ... ...

Abstract	SLC25A32 is a member of the solute carrier 25 family of mitochondrial transporters. SLC25A32 transports tetrahydrofolate (THF) as well as FAD into mitochondria and regulates mitochondrial one-carbon metabolism and redox balance. While it is known that cancer cells require one-carbon and FAD-dependent mitochondrial metabolism to sustain cell proliferation, the role of SLC25A32 in cancer cell growth remains unexplored. Our results indicate that the
Language	English
Publishing date	2020-02-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.27486
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Book ; Online ; Thesis: Brk tyrosine kinase signaling in the gastrointestinal tract

Hägebarth, Andrea

2005

Author's details	von Andrea Hägebarth
Language	English
Size	Online-Ressource
Document type	Book ; Online ; Thesis
Thesis / German Habilitation thesis	Humboldt-Univ., Diss--Berlin, 2005
Database	Former special subject collection: coastal and deep sea fishing

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Article ; Online: Functional diversity of inhibitors tackling the differentiation blockage of MLL-rearranged leukemia.

Brzezinka, Krzysztof / Nevedomskaya, Ekaterina / Lesche, Ralf / Steckel, Michael / Eheim, Ashley L / Haegebarth, Andrea / Stresemann, Carlo

Journal of hematology & oncology

2019 Volume 12, Issue 1, Page(s) 66

Abstract: Introduction: The chromosomal rearrangements of the mixed-lineage leukemia gene MLL (KMT2A) have been extensively characterized as a potent oncogenic driver in leukemia. For its oncogenic function, most MLL-fusion proteins exploit the multienzyme super ... ...

Abstract	Introduction: The chromosomal rearrangements of the mixed-lineage leukemia gene MLL (KMT2A) have been extensively characterized as a potent oncogenic driver in leukemia. For its oncogenic function, most MLL-fusion proteins exploit the multienzyme super elongation complex leading to elevated expression of MLL target genes. High expression of MLL target genes overwrites the normal hematopoietic differentiation program, resulting in undifferentiated blasts characterized by the capacity to self-renew. Although extensive resources devoted to increased understanding of therapeutic targets to overcome de-differentiation in ALL/AML, the inter-dependencies of targets are still not well described. The majority of inhibitors potentially interfering with MLL-fusion protein driven transformation have been characterized in individual studies, which so far hindered their direct cross-comparison. Methods: In our study, we characterized head-to-head clinical stage inhibitors for BET, DHODH, DOT1L as well as two novel inhibitors for CDK9 and the Menin-MLL interaction with a focus on differentiation induction. We profiled those inhibitors for global gene expression effects in a large cell line panel and examined cellular responses such as inhibition of proliferation, apoptosis induction, cell cycle arrest, surface marker expression, morphological phenotype changes, and phagocytosis as functional differentiation readout. We also verified the combination potential of those inhibitors on proliferation and differentiation level. Results: Our analysis revealed significant differences in differentiation induction and in modulating MLL-fusion target gene expression. We observed Menin-MLL and DOT1L inhibitors act very specifically on MLL-fused leukemia cell lines, whereas inhibitors of BET, DHODH and P-TEFb have strong effects beyond MLL-fusions. Significant differentiation effects were detected for Menin-MLL, DOT1L, and DHODH inhibitors, whereas BET and CDK9 inhibitors primarily induced apoptosis in AML/ALL cancer models. For the first time, we explored combination potential of the abovementioned inhibitors with regards to overcoming the differentiation blockage. Conclusion: Our findings show substantial diversity in the molecular activities of those inhibitors and provide valuable insights into the further developmental potential as single agents or in combinations in MLL-fused leukemia.
MeSH term(s)	Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Enzyme Inhibitors/chemistry ; Enzyme Inhibitors/pharmacology ; Gene Expression Regulation, Leukemic/drug effects ; Gene Rearrangement/drug effects ; Histone-Lysine N-Methyltransferase/genetics ; Histone-Lysine N-Methyltransferase/metabolism ; Humans ; Leukemia/drug therapy ; Leukemia/genetics ; Leukemia/metabolism ; Myeloid-Lymphoid Leukemia Protein/genetics ; Myeloid-Lymphoid Leukemia Protein/metabolism ; Oncogene Proteins, Fusion/genetics ; Oncogene Proteins, Fusion/metabolism ; Protein Interaction Maps/drug effects ; Proto-Oncogene Proteins/metabolism
Chemical Substances	Antineoplastic Agents ; Enzyme Inhibitors ; KMT2A protein, human ; MEN1 protein, human ; Oncogene Proteins, Fusion ; Proto-Oncogene Proteins ; Myeloid-Lymphoid Leukemia Protein (149025-06-9) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43)
Language	English
Publishing date	2019-06-28
Publishing country	England
Document type	Journal Article
ZDB-ID	2429631-4
ISSN	1756-8722 ; 1756-8722
ISSN (online)	1756-8722
ISSN	1756-8722
DOI	10.1186/s13045-019-0749-y
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Article ; Online: Wnt signaling, lgr5, and stem cells in the intestine and skin.

Haegebarth, Andrea / Clevers, Hans

The American journal of pathology

2009 Volume 174, Issue 3, Page(s) 715–721

Abstract: Stem cells hold great promise for regenerative medicine, but have remained elusive in many tissues because of a lack of adequate definitive markers. Progress in mouse genetics has provided the tools for characterization and validation of stem cell ... ...

Abstract	Stem cells hold great promise for regenerative medicine, but have remained elusive in many tissues because of a lack of adequate definitive markers. Progress in mouse genetics has provided the tools for characterization and validation of stem cell markers by functional and/or lineage tracing assays. The Wnt target gene Lgr5 has been recently identified as a novel stem cell marker of the intestinal epithelium and the hair follicle. In the intestine, Lgr5 is exclusively expressed in cycling crypt base columnar cells. Genetic lineage-tracing experiments revealed that crypt base columnar cells are capable of self-renewal and multipotency, thus representing genuine intestinal stem cells. In the stem cell niche of the murine hair follicle, Lgr5 is expressed in actively cycling cells. Transplantation and lineage tracing experiments have demonstrated that these Lgr5(+ve) cells maintain all cell lineages of the hair follicle throughout long periods of time and can build entire new hair follicles. Expression of Lgr5 in multiple other organs indicates that it may represent a global marker of adult stem cells. This review attempts to provide a comprehensive overview of the stem cell compartments in the intestine and skin with a focus on the cycling, yet long-lived and multipotent, Lgr5(+ve) stem cell populations.
MeSH term(s)	Animals ; Cell Division ; Digestion ; Genetic Markers ; Hair Follicle/cytology ; Hair Follicle/physiology ; Humans ; Intestinal Mucosa/cytology ; Intestinal Mucosa/physiology ; Intestines/cytology ; Intestines/physiology ; Mice ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/physiology ; Skin/cytology ; Skin Physiological Phenomena ; Stem Cells/cytology ; Stem Cells/physiology ; Wnt Proteins/physiology
Chemical Substances	Genetic Markers ; LGR5 protein, human ; Lgr5 protein, mouse ; Receptors, G-Protein-Coupled ; Wnt Proteins
Language	English
Publishing date	2009-02-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.2353/ajpath.2009.080758
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Book ; Online ; Thesis: Brk tyrosine kinase signaling in the gastrointestinal tract

Hägebarth, Andrea [Verfasser]

2005

Author's details	von Andrea Hägebarth
Keywords	Medizin, Gesundheit ; Medicine, Health
Subject code	sg610
Language	English
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article: Characterization of the Menin-MLL Interaction as Therapeutic Cancer Target.

Brzezinka, Krzysztof / Nevedomskaya, Ekaterina / Lesche, Ralf / Haegebarth, Andrea / Ter Laak, Antonius / Fernández-Montalván, Amaury E / Eberspaecher, Uwe / Werbeck, Nicolas D / Moenning, Ursula / Siegel, Stephan / Haendler, Bernard / Eheim, Ashley L / Stresemann, Carlo

Cancers

2020 Volume 12, Issue 1

Abstract: Inhibiting the interaction of menin with the histone methyltransferase MLL1 (KMT2A) has recently emerged as a novel therapeutic strategy. Beneficial therapeutic effects have been postulated in leukemia, prostate, breast, liver and in synovial sarcoma ... ...

Abstract	Inhibiting the interaction of menin with the histone methyltransferase MLL1 (KMT2A) has recently emerged as a novel therapeutic strategy. Beneficial therapeutic effects have been postulated in leukemia, prostate, breast, liver and in synovial sarcoma models. In those indications, MLL1 recruitment by menin was described to critically regulate the expression of disease associated genes. However, most findings so far rely on single study reports. Here we independently evaluated the pathogenic functions of the menin-MLL interaction in a large set of different cancer models with a potent and selective probe inhibitor BAY-155. We characterized the inhibition of the menin-MLL interaction for anti-proliferation, gene transcription effects, and for efficacy in several in vivo xenografted tumor models. We found a specific therapeutic activity of BAY-155 primarily in AML/ALL models. In solid tumors, we observed anti-proliferative effects of BAY-155 in a surprisingly limited fraction of cell line models. These findings were further validated in vivo. Overall, our study using a novel, highly selective and potent inhibitor, shows that the menin-MLL interaction is not essential for the survival of most solid cancer models. We can confirm that disrupting the menin-MLL complex has a selective therapeutic benefit in MLL-fused leukemia. In solid cancers, effects are restricted to single models and more limited than previously claimed.
Language	English
Publishing date	2020-01-14
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers12010201
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Article ; Online: Synergistic activity of IDH1 inhibitor BAY1436032 with azacitidine in IDH1 mutant acute myeloid leukemia.

Chaturvedi, Anuhar / Gupta, Charu / Gabdoulline, Razif / Borchert, Nora M / Goparaju, Ramya / Kaulfuss, Stefan / Görlich, Kerstin / Schottmann, Renate / Othman, Basem / Welzenbach, Julia / Panknin, Olaf / Wagner, Markus / Geffers, Robert / Ganser, Arnold / Thol, Felicitas / Jeffers, Michael / Haegebarth, Andrea / Heuser, Michael

Haematologica

2021 Volume 106, Issue 2, Page(s) 565–573

Abstract: Mutant IDH1 (mIDH1) inhibitors have shown single-agent activity in relapsed/refractory AML, though most patients eventually relapse. We evaluated the efficacy and molecular mechanism of the combination treatment with azacitidine, which is currently the ... ...

Abstract	Mutant IDH1 (mIDH1) inhibitors have shown single-agent activity in relapsed/refractory AML, though most patients eventually relapse. We evaluated the efficacy and molecular mechanism of the combination treatment with azacitidine, which is currently the standard of care in older AML patients, and mIDH1 inhibitor BAY1436032. Both compounds were evaluated in vivo as single agents and in combination with sequential (azacitidine, followed by BAY1436032) or simultaneous application in two human IDH1 mutated AML xenograft models. Combination treatment significantly prolonged survival compared to single agent or control treatment (P<.005). The sequential combination treatment depleted leukemia stem cells (LSC) by 470-fold. Interestingly, the simultaneous combination treatment depleted LSCs by 33,150-fold compared to control mice. This strong synergy is mediated through inhibition of MAPK/ERK and RB/E2F signaling. Our data strongly argues for the concurrent application of mIDH1 inhibitors and azacitidine and predicts improved outcome of this regimen in IDH1 mutated AML patients.
MeSH term(s)	Aged ; Aniline Compounds ; Animals ; Azacitidine ; Benzimidazoles ; Humans ; Isocitrate Dehydrogenase/genetics ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/genetics ; Mice
Chemical Substances	Aniline Compounds ; BAY 1436032 ; Benzimidazoles ; Isocitrate Dehydrogenase (EC 1.1.1.41) ; IDH1 protein, human (EC 1.1.1.42.) ; Azacitidine (M801H13NRU)
Language	English
Publishing date	2021-02-01
Publishing country	Italy
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2019.236992
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Article ; Online: Identification of KCa3.1 Channel as a Novel Regulator of Oxidative Phosphorylation in a Subset of Pancreatic Carcinoma Cell Lines.

Kovalenko, Ilya / Glasauer, Andrea / Schöckel, Laura / Sauter, Daniel R P / Ehrmann, Alexander / Sohler, Florian / Hägebarth, Andrea / Novak, Ivana / Christian, Sven

PloS one

2016 Volume 11, Issue 8, Page(s) e0160658

Abstract: Pancreatic ductal adenocarcinoma (PDAC) represents the most common form of pancreatic cancer with rising incidence in developing countries and overall 5-year survival rates of less than 5%. The most frequent mutations in PDAC are gain-of-function ... ...

Abstract	Pancreatic ductal adenocarcinoma (PDAC) represents the most common form of pancreatic cancer with rising incidence in developing countries and overall 5-year survival rates of less than 5%. The most frequent mutations in PDAC are gain-of-function mutations in KRAS as well as loss-of-function mutations in p53. Both mutations have severe impacts on the metabolism of tumor cells. Many of these metabolic changes are mediated by transporters or channels that regulate the exchange of metabolites and ions between the intracellular compartment and the tumor microenvironment. In the study presented here, our goal was to identify novel transporters or channels that regulate oxidative phosphorylation (OxPhos) in PDAC in order to characterize novel potential drug targets for the treatment of these cancers. We set up a Seahorse Analyzer XF based siRNA screen and identified previously described as well as novel regulators of OxPhos. The siRNA that resulted in the greatest change in cellular oxygen consumption was targeting the KCNN4 gene, which encodes for the Ca2+-sensitive K+ channel KCa3.1. This channel has not previously been reported to regulate OxPhos. Knock-down experiments as well as the use of a small molecule inhibitor confirmed its role in regulating oxygen consumption, ATP production and cellular proliferation. Furthermore, PDAC cell lines sensitive to KCa3.1 inhibition were shown to express the channel protein in the plasma membrane as well as in the mitochondria. These differences in the localization of KCa3.1 channels as well as differences in the regulation of cellular metabolism might offer opportunities for targeted therapy in subsets of PDAC.
MeSH term(s)	Apoptosis ; Carcinoma, Pancreatic Ductal/metabolism ; Carcinoma, Pancreatic Ductal/pathology ; Cell Proliferation ; Gene Expression Regulation, Neoplastic ; Humans ; Intermediate-Conductance Calcium-Activated Potassium Channels/metabolism ; Oxidative Phosphorylation ; Pancreatic Neoplasms/metabolism ; Pancreatic Neoplasms/pathology ; Signal Transduction ; Tumor Cells, Cultured
Chemical Substances	Intermediate-Conductance Calcium-Activated Potassium Channels ; KCNN4 protein, human
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0160658
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Metabolic pathway analyses identify proline biosynthesis pathway as a promoter of liver tumorigenesis.

Ding, Zhaobing / Ericksen, Russell E / Escande-Beillard, Nathalie / Lee, Qian Yi / Loh, Abigail / Denil, Simon / Steckel, Michael / Haegebarth, Andrea / Wai Ho, Timothy Shen / Chow, Pierce / Toh, Han Chong / Reversade, Bruno / Gruenewald, Sylvia / Han, Weiping

Journal of hepatology

2019 Volume 72, Issue 4, Page(s) 725–735

Abstract: Background & aim: Under the regulation of various oncogenic pathways, cancer cells undergo adaptive metabolic programming to maintain specific metabolic states that support their uncontrolled proliferation. As it has been difficult to directly and ... ...

Abstract	Background & aim: Under the regulation of various oncogenic pathways, cancer cells undergo adaptive metabolic programming to maintain specific metabolic states that support their uncontrolled proliferation. As it has been difficult to directly and effectively inhibit oncogenic signaling cascades with pharmaceutical compounds, focusing on the downstream metabolic pathways that enable indefinite growth may provide therapeutic opportunities. Thus, we sought to characterize metabolic changes in hepatocellular carcinoma (HCC) development and identify metabolic targets required for tumorigenesis. Methods: We compared gene expression profiles of Morris Hepatoma (MH3924a) and DEN (diethylnitrosamine)-induced HCC models to those of liver tissues from normal and rapidly regenerating liver models, and performed gain- and loss-of-function studies of the identified gene targets for their roles in cancer cell proliferation in vitro and in vivo. Results: The proline biosynthetic enzyme PYCR1 (pyrroline-5-carboxylate reductase 1) was identified as one of the most upregulated genes in the HCC models. Knockdown of PYCR1 potently reduced cell proliferation of multiple HCC cell lines in vitro and tumor growth in vivo. Conversely, overexpression of PYCR1 enhanced the proliferation of the HCC cell lines. Importantly, PYCR1 expression was not elevated in the regenerating liver, and KD or overexpression of PYCR1 had no effect on proliferation of non-cancerous cells. Besides PYCR1, we found that additional proline biosynthetic enzymes, such as ALDH18A1, were upregulated in HCC models and also regulated HCC cell proliferation. Clinical data demonstrated that PYCR1 expression was increased in HCC, correlated with tumor grade, and was an independent predictor of clinical outcome. Conclusion: Enhanced expression of proline biosynthetic enzymes promotes HCC cell proliferation. Inhibition of PYCR1 or ALDH18A1 may be a novel therapeutic strategy to target HCC. Lay summary: Even with the recently approved immunotherapies against liver cancer, currently available medications show limited clinical benefits or efficacy in the majority of patients. As such, it remains a top priority to discover new targets for effective liver cancer treatment. Here, we identify a critical role for the proline biosynthetic pathway in liver cancer development, and demonstrate that targeting key proteins in the pathway, namely PYCR1 and ALDH18A1, may be a novel therapeutic strategy for liver cancer.
MeSH term(s)	Aldehyde Dehydrogenase/deficiency ; Aldehyde Dehydrogenase/genetics ; Animals ; Carcinogenesis/genetics ; Carcinogenesis/metabolism ; Carcinoma, Hepatocellular/chemically induced ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology ; Cell Proliferation/genetics ; Diethylnitrosamine/adverse effects ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; HEK293 Cells ; HaCaT Cells ; Hep G2 Cells ; Humans ; Liver Neoplasms/chemically induced ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; Liver Neoplasms, Experimental/genetics ; Liver Neoplasms, Experimental/metabolism ; Liver Neoplasms, Experimental/pathology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Nude ; Mice, SCID ; Proline/biosynthesis ; Pyrroline Carboxylate Reductases/deficiency ; Pyrroline Carboxylate Reductases/genetics ; Rats ; Signal Transduction/genetics ; Transcriptome ; Transfection ; Tumor Burden/genetics ; Xenograft Model Antitumor Assays ; delta-1-Pyrroline-5-Carboxylate Reductase
Chemical Substances	Diethylnitrosamine (3IQ78TTX1A) ; Proline (9DLQ4CIU6V) ; ALDH18A1 protein, human (EC 1.2.1.3) ; Aldehyde Dehydrogenase (EC 1.2.1.3) ; Pyrroline Carboxylate Reductases (EC 1.5.1.-)
Language	English
Publishing date	2019-11-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2019.10.026
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Article ; Online: Discovery and Characterization of the Potent and Highly Selective 1,7-Naphthyridine-Based Inhibitors BAY-091 and BAY-297 of the Kinase PIP4K2A.

Journal of medicinal chemistry

2021 Volume 64, Issue 21, Page(s) 15883–15911

Abstract: PIP4K2A is an insufficiently studied type II lipid kinase that catalyzes the conversion of phosphatidylinositol-5-phosphate (PI5P) into phosphatidylinositol 4,5-bisphosphate (PI4, ... ...

Abstract	PIP4K2A is an insufficiently studied type II lipid kinase that catalyzes the conversion of phosphatidylinositol-5-phosphate (PI5P) into phosphatidylinositol 4,5-bisphosphate (PI4,5P
MeSH term(s)	Animals ; Apoptosis/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Drug Discovery ; Drug Screening Assays, Antitumor ; Enzyme Inhibitors/chemistry ; Enzyme Inhibitors/pharmacology ; High-Throughput Screening Assays ; Humans ; Mice ; Mice, Knockout ; Mitochondria/drug effects ; Mitochondria/metabolism ; Naphthyridines/chemistry ; Phosphotransferases (Alcohol Group Acceptor)/antagonists & inhibitors ; Phosphotransferases (Alcohol Group Acceptor)/genetics ; Reactive Oxygen Species/metabolism ; Signal Transduction/drug effects ; Structure-Activity Relationship
Chemical Substances	Enzyme Inhibitors ; Naphthyridines ; Reactive Oxygen Species ; PIP4K2A protein, human (EC 2.7.1.-) ; Phosphotransferases (Alcohol Group Acceptor) (EC 2.7.1.-)
Language	English
Publishing date	2021-10-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	218133-2
ISSN	1520-4804 ; 0022-2623
ISSN (online)	1520-4804
ISSN	0022-2623
DOI	10.1021/acs.jmedchem.1c01245
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