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Article ; Online: The tumour suppressor Pdcd4: recent advances in the elucidation of function and regulation.

Lankat-Buttgereit, Brigitte / Göke, Rüdiger

2009 Volume 101, Issue 6, Page(s) 309–317

Abstract: Pdcd4 (programmed cell death 4) has been known as a tumour suppressor gene and potential target for anticancer therapies for several years. Initially, Pdcd4 was identified as a gene that is up-regulated during apoptosis, but its precise role still ... ...

Abstract	Pdcd4 (programmed cell death 4) has been known as a tumour suppressor gene and potential target for anticancer therapies for several years. Initially, Pdcd4 was identified as a gene that is up-regulated during apoptosis, but its precise role still remains to be defined. However, there is increasing evidence that Pdcd4 levels influence transcription, as well as translation, modulate different signal transduction pathways and might act as a tumour suppressor. Interestingly, recent data suggest that Pdcd4 function may depend on cell type and/or genetic background. This review summarizes the current knowledge regarding the function and regulation of Pdcd4.
MeSH term(s)	Animals ; Apoptosis Regulatory Proteins/genetics ; Apoptosis Regulatory Proteins/metabolism ; Genes, Tumor Suppressor ; Humans ; Neoplasms/drug therapy ; Neoplasms/metabolism ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Signal Transduction
Chemical Substances	Apoptosis Regulatory Proteins ; PDCD4 protein, human ; RNA-Binding Proteins
Language	English
Publishing date	2009-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	245745-3
ISSN	1768-322X ; 0399-0311 ; 0248-4900
ISSN (online)	1768-322X
ISSN	0399-0311 ; 0248-4900
DOI	10.1042/BC20080191
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Article ; Online: Inactivation of PRIM1 Function Sensitizes Cancer Cells to ATR and CHK1 Inhibitors.

Job, Albert / Schmitt, Lisa-Maria / von Wenserski, Lisa / Lankat-Buttgereit, Brigitte / Gress, Thomas M / Buchholz, Malte / Gallmeier, Eike

Neoplasia (New York, N.Y.)

2018 Volume 20, Issue 11, Page(s) 1135–1143

Abstract: The phosphoinositide 3-kinase-related kinase ATR is a central regulator of the DNA damage response. Its chemical inhibition eliminates subsets of cancer cells in various tumor types. This effect is caused at least partly by the synthetically lethal ... ...

Abstract	The phosphoinositide 3-kinase-related kinase ATR is a central regulator of the DNA damage response. Its chemical inhibition eliminates subsets of cancer cells in various tumor types. This effect is caused at least partly by the synthetically lethal relationship between ATR and certain DNA repair genes. In a previous screen using an siRNA library against DNA repair genes, we identified PRIM1, a part of the polymerase α-primase complex, as acting synthetically lethal with ATR. Applying a genetic ATR knock-in model of colorectal cancer cells, we confirmed that PRIM1 depletion inhibited proliferation of ATR-deficient cells and excluded artifacts due to clonal variation using an ATR reexpressing cell clone. We expanded these data by demonstrating in different cell lines that also chemical inhibition of ATR or its main effector kinase CHK1 reduces proliferation upon depletion of PRIM1. Mechanistically, PRIM1 depletion in ATR-deficient cells caused S-phase stasis in the absence of increased DNA damage followed by Wee1-mediated activation of caspase 8 and apoptosis. As PRIM1 inactivation sensitizes cancer cells to ATR and CHK1 inhibitors, mutations in PRIM1 or other components of the polymerase α-primase complex could represent novel targets for individualized tumor therapeutic approaches using ATR/CHK1 inhibitors, as has been previously demonstrated for POLD1, the catalytic subunit of polymerase δ.
MeSH term(s)	Apoptosis/drug effects ; Apoptosis/genetics ; Ataxia Telangiectasia Mutated Proteins/antagonists & inhibitors ; Ataxia Telangiectasia Mutated Proteins/genetics ; Cell Cycle/drug effects ; Cell Cycle/genetics ; Cell Line, Tumor ; Cell Proliferation ; Checkpoint Kinase 1/antagonists & inhibitors ; DNA Primase/antagonists & inhibitors ; Drug Resistance, Neoplasm ; Gene Expression ; Histones/metabolism ; Humans ; Protein Kinase Inhibitors/pharmacology ; RNA Interference ; RNA, Small Interfering/genetics ; Synthetic Lethal Mutations
Chemical Substances	Histones ; Protein Kinase Inhibitors ; RNA, Small Interfering ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; Checkpoint Kinase 1 (EC 2.7.11.1) ; DNA Primase (EC 2.7.7.-) ; PRIM1 protein, human (EC 2.7.7.-)
Language	English
Publishing date	2018-09-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	1483840-0
ISSN	1476-5586 ; 1522-8002
ISSN (online)	1476-5586
ISSN	1522-8002
DOI	10.1016/j.neo.2018.08.009
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Article ; Online: The POLD1

Job, Albert / Tatura, Marina / Schäfer, Cora / Lutz, Veronika / Schneider, Hanna / Lankat-Buttgereit, Brigitte / Zielinski, Alexandra / Borgmann, Kerstin / Bauer, Christian / Gress, Thomas M / Buchholz, Malte / Gallmeier, Eike

Scientific reports

2020 Volume 10, Issue 1, Page(s) 18924

Abstract: Inhibition of the kinase ATR, a central regulator of the DNA damage response, eliminates subsets of cancer cells in certain tumors. As previously shown, this is at least partly attributable to synthetic lethal interactions between ATR and POLD1, the ... ...

Abstract	Inhibition of the kinase ATR, a central regulator of the DNA damage response, eliminates subsets of cancer cells in certain tumors. As previously shown, this is at least partly attributable to synthetic lethal interactions between ATR and POLD1, the catalytic subunit of the polymerase δ. Various POLD1 variants have been found in colorectal cancer, but their significance as therapeutic targets for ATR pathway inhibition remains unknown. Using CRISPR/Cas9 in the colorectal cancer cell line DLD-1, which harbors four POLD1 variants, we established heterozygous POLD1-knockout clones with exclusive expression of distinct variants to determine the functional relevance of these variants individually by assessing their impact on ATR pathway activation, DNA replication, and cellular sensitivity to inhibition of ATR or its effector kinase CHK1. Of the four variants analyzed, only POLD1
MeSH term(s)	Amino Acid Substitution ; Animals ; CRISPR-Cas Systems ; Cell Line, Tumor ; Cell Survival/drug effects ; Checkpoint Kinase 1/antagonists & inhibitors ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; DNA Polymerase III/genetics ; DNA Replication/drug effects ; Gene Knockout Techniques ; Humans ; Mice ; Pyrimidines/administration & dosage ; Pyrimidines/pharmacology ; Sulfoxides/administration & dosage ; Sulfoxides/pharmacology ; Xenograft Model Antitumor Assays
Chemical Substances	Pyrimidines ; Sulfoxides ; ceralasertib (85RE35306Z) ; CHEK1 protein, human (EC 2.7.11.1) ; Checkpoint Kinase 1 (EC 2.7.11.1) ; POLD1 protein, human (EC 2.7.7.-) ; DNA Polymerase III (EC 2.7.7.7)
Language	English
Publishing date	2020-11-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-76033-1
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Article ; Online: The FGFR Inhibitor NVP-BGJ398 Induces NSCLC Cell Death by Activating Caspase-dependent Pathways as well as Caspase-independent Apoptosis.

Göke, Antonia / Göke, Rüdiger / Ofner, Andrea / Herbst, Andreas / Lankat-Buttgereit, Brigitte

Anticancer research

2015 Volume 35, Issue 11, Page(s) 5873–5879

Abstract: Background: Fibroblast growth factor receptors are expressed in diverse cell types. They play a critical role in tumor development. Their activation promotes cell-cycle progression, angiogenesis, and cell survival by induction/suppression of the ... ...

Abstract	Background: Fibroblast growth factor receptors are expressed in diverse cell types. They play a critical role in tumor development. Their activation promotes cell-cycle progression, angiogenesis, and cell survival by induction/suppression of the expression of proteins involved. Materials and methods: Non-small cell lung cancer (NSCLC) cells (line H1581) were treated with NVP-BGJ398 to evaluate effects on growth by western blot, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide assay and cell-cycle analysis. Results: NVP-BGJ398 induced cell death in H1581 cells by activating caspase-dependent mitochondrial and non-mitochondrial pathways. Caspase-independent apoptosis was also activated. Cells were found to be arrested in the G0/G1 phase. Furthermore, the expression of the tumor-suppressor gene programmed cell death 4 (PDCD4) was up-regulated with suppression of angiopoietin 2 (ANG2). This represents an additional mechanism by which NVP-BGJ389 inhibits tumor growth. Conclusion: Various pathways induce apoptosis in NSCLC cells by employing NVP-BGJ398. These data reflect the potential of cancer treatment utilizing small FGFR inhibitors.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Blotting, Western ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/metabolism ; Carcinoma, Non-Small-Cell Lung/pathology ; Caspases/metabolism ; Cell Cycle/drug effects ; Cell Proliferation/drug effects ; Gene Expression Regulation, Enzymologic/drug effects ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Phenylurea Compounds/pharmacology ; Pyrimidines/pharmacology ; Receptor, Fibroblast Growth Factor, Type 1/antagonists & inhibitors ; Tumor Cells, Cultured
Chemical Substances	Antineoplastic Agents ; Phenylurea Compounds ; Pyrimidines ; infigratinib (A4055ME1VK) ; FGFR1 protein, human (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 1 (EC 2.7.10.1) ; Caspases (EC 3.4.22.-)
Language	English
Publishing date	2015-10-22
Publishing country	Greece
Document type	Journal Article
ZDB-ID	604549-2
ISSN	1791-7530 ; 0250-7005
ISSN (online)	1791-7530
ISSN	0250-7005
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Article: A comparison of three (67/68)Ga-labelled exendin-4 derivatives for β-cell imaging on the GLP-1 receptor: the influence of the conjugation site of NODAGA as chelator.

Jodal, Andreas / Lankat-Buttgereit, Brigitte / Brom, Maarten / Schibli, Roger / Béhé, Martin

EJNMMI research

2014 Volume 4, Page(s) 31

Abstract: Background: Various diseases derive from pathologically altered β-cells. Their function can be increased, leading to hyperinsulinism, or decreased, resulting in diabetes. Non-invasive imaging of the β-cell-specific glucagon-like peptide receptor-1 (GLP- ... ...

Abstract	Background: Various diseases derive from pathologically altered β-cells. Their function can be increased, leading to hyperinsulinism, or decreased, resulting in diabetes. Non-invasive imaging of the β-cell-specific glucagon-like peptide receptor-1 (GLP-1R) would allow the assessment of both β-cell mass and derived tumours, potentially improving the diagnosis of various conditions. We tested three new (67/68)Ga-labelled derivatives of exendin-4, an agonist of GLP-1R, in vitro and in vivo. We determined the influence of the chelator NODAGA conjugated to resident lysines either at positions 12 and 27 or the C-terminally attached lysine at position 40 on the binding and kinetics of the peptide. Methods: Binding and internalisation of (67)Ga-labelled Ex4NOD12, Ex4NOD27 and Ex4NOD40 were tested on Chinese hamster lung (CHL) cells stably transfected to express the GLP-1 receptor (GLP-1R). In vivo biodistribution of (68)Ga-labelled peptides was investigated in CD1 nu/nu mice with subcutaneous CHL-GLP-1R positive tumours; the specificity of the binding to GLP-1R was determined by pre-injecting excess peptide. Results: All peptides showed good in vitro binding affinities to GLP-1R in the range of 29 to 54 nM. (67/68)Ga-Ex4NOD40 and (67/68)Ga-Ex4NOD12 show excellent internalisation (>30%) and high specific uptake in GLP-1R positive tissue, but high activity was also found in the kidneys. Conclusions: We show that of the three peptides, Ga-Ex4NOD40 and Ga-Ex4NOD12 demonstrate the most favourable in vitro properties and in vivo binding to GLP-1R positive tissue. Therefore, we conclude that the lysines at positions 12 and 40 might preferentially be utilised for modifying exendin-4.
Language	English
Publishing date	2014-06-22
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2619892-7
ISSN	2191-219X
ISSN	2191-219X
DOI	10.1186/s13550-014-0031-9
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Article: Programmed cell death protein 4 (pdcd4): a novel target for antineoplastic therapy?

Lankat-Buttgereit, Brigitte / Göke, Rüdiger

Biology of the cell

2003 Volume 95, Issue 8, Page(s) 515–519

Abstract: Pdcd4 is a novel gene first identified as a differentially expressed protein during apoptosis. In the meantime not only the impact of Pdcd4 in programmed cell death but also an implication in transformation suppression by inhibition of protein ... ...

Abstract	Pdcd4 is a novel gene first identified as a differentially expressed protein during apoptosis. In the meantime not only the impact of Pdcd4 in programmed cell death but also an implication in transformation suppression by inhibition of protein translation is discussed. These features implicate a potential value of Pdcd4 as a molecular target in cancer therapy. This review summarizes the current knowledge about expression, structure and function of Pdcd4.
MeSH term(s)	Animals ; Apoptosis ; Apoptosis Regulatory Proteins ; Eukaryotic Initiation Factor-4G/metabolism ; Mice ; Neoplasms/therapy ; RNA-Binding Proteins/antagonists & inhibitors ; RNA-Binding Proteins/chemistry ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/physiology ; Tumor Suppressor Proteins/antagonists & inhibitors ; Tumor Suppressor Proteins/chemistry ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/physiology ; Up-Regulation
Chemical Substances	Apoptosis Regulatory Proteins ; Eukaryotic Initiation Factor-4G ; Pdcd4 protein, mouse ; RNA-Binding Proteins ; Tumor Suppressor Proteins
Language	English
Publishing date	2003-10-24
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	245745-3
ISSN	1768-322X ; 0248-4900 ; 0399-0311
ISSN (online)	1768-322X
ISSN	0248-4900 ; 0399-0311
DOI	10.1016/j.biolcel.2003.09.003
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Article ; Online: The POLD1R689W variant increases the sensitivity of colorectal cancer cells to ATR and CHK1 inhibitors

Albert Job / Marina Tatura / Cora Schäfer / Veronika Lutz / Hanna Schneider / Brigitte Lankat-Buttgereit / Alexandra Zielinski / Kerstin Borgmann / Christian Bauer / Thomas M. Gress / Malte Buchholz / Eike Gallmeier

Scientific Reports, Vol 10, Iss 1, Pp 1-

2020 Volume 12

Abstract: Abstract Inhibition of the kinase ATR, a central regulator of the DNA damage response, eliminates subsets of cancer cells in certain tumors. As previously shown, this is at least partly attributable to synthetic lethal interactions between ATR and POLD1, ...

Abstract	Abstract Inhibition of the kinase ATR, a central regulator of the DNA damage response, eliminates subsets of cancer cells in certain tumors. As previously shown, this is at least partly attributable to synthetic lethal interactions between ATR and POLD1, the catalytic subunit of the polymerase δ. Various POLD1 variants have been found in colorectal cancer, but their significance as therapeutic targets for ATR pathway inhibition remains unknown. Using CRISPR/Cas9 in the colorectal cancer cell line DLD-1, which harbors four POLD1 variants, we established heterozygous POLD1-knockout clones with exclusive expression of distinct variants to determine the functional relevance of these variants individually by assessing their impact on ATR pathway activation, DNA replication, and cellular sensitivity to inhibition of ATR or its effector kinase CHK1. Of the four variants analyzed, only POLD1R689W affected POLD1 function, as demonstrated by compensatory ATR pathway activation and impaired DNA replication. Upon treatment with ATR or CHK1 inhibitors, POLD1R689W strongly decreased cell survival in vitro, which was attributable at least partly to S phase impairment and apoptosis. Similarly, treatment with the ATR inhibitor AZD6738 inhibited growth of murine xenograft tumors, harboring the POLD1R689W variant, in vivo. Our POLD1-knockout model thus complements algorithm-based models to predict the pathogenicity of tumor-specific variants of unknown significance and illustrates a novel and potentially clinically relevant therapeutic approach using ATR/CHK1 inhibitors in POLD1-deficient tumors.
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publishing date	2020-11-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: The transporter associated with antigen processing: function and implications in human diseases.

Lankat-Buttgereit, Brigitte / Tampé, Robert

Physiological reviews

2002 Volume 82, Issue 1, Page(s) 187–204

Abstract: The adaptive immune systems have evolved to protect the organism against pathogens encountering the host. Extracellular occurring viruses or bacteria are mainly bound by antibodies from the humoral branch of the immune response, whereas infected or ... ...

Abstract	The adaptive immune systems have evolved to protect the organism against pathogens encountering the host. Extracellular occurring viruses or bacteria are mainly bound by antibodies from the humoral branch of the immune response, whereas infected or malignant cells are identified and eliminated by the cellular immune system. To enable the recognition, proteins are cleaved into peptides in the cytosol and are presented on the cell surface by class I molecules of the major histocompatibility complex (MHC). The transport of the antigenic peptides into the lumen of the endoplasmic reticulum (ER) and loading onto the MHC class I molecules is an essential process for the presentation to cytotoxic T lymphocytes. The delivery of these peptides is performed by the transporter associated with antigen processing (TAP). TAP is a heterodimer of TAP1 and TAP2, each subunit containing transmembrane domains and an ATP-binding motif. Sequence homology analysis revealed that TAP belongs to the superfamily of ATP-binding cassette transporters. Loss of TAP function leads to a loss of cell surface expression of MHC class I molecules. This may be a strategy for tumors and virus-infected cells to escape immune surveillance. Structure and function of the TAP complex as well as the implications of loss or downregulation of TAP is the topic of this review.
MeSH term(s)	ATP-Binding Cassette Sub-Family B Member 2 ; ATP-Binding Cassette Transporters/physiology ; ATP-Binding Cassette, Sub-Family B, Member 3 ; Animals ; Autoimmune Diseases/physiopathology ; Down-Regulation ; Humans ; Immunity/physiology ; Neoplasms/etiology ; Virus Diseases/physiopathology
Chemical Substances	ATP-Binding Cassette Sub-Family B Member 2 ; ATP-Binding Cassette, Sub-Family B, Member 3 ; TAP1 protein, human ; TAP2 protein, human (145892-13-3)
Language	English
Publishing date	2002-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	209902-0
ISSN	1522-1210 ; 0031-9333
ISSN (online)	1522-1210
ISSN	0031-9333
DOI	10.1152/physrev.00025.2001
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Book ; Online ; Thesis: Die Wirkung von Pioglitazon auf das Proteom einer humanen neuroendokrinen Pankreaskarzinom-Zelllinie

Müller, Sabine [Verfasser] / Lankat-Buttgereit, Brigitte [Akademischer Betreuer]

2011

Author's details	Sabine Müller. Betreuer: Brigitte Lankat-Buttgereit
Keywords	Medizin, Gesundheit ; Medicine, Health
Subject code	sg610
Language	German
Publisher	Philipps-Universität Marburg
Publishing place	Marburg
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article ; Online: Expression of programmed cell death protein 4 (PDCD4) and miR-21 in urothelial carcinoma.

Fischer, Nicolas / Göke, Friederike / Splittstösser, Vera / Lankat-Buttgereit, Brigitte / Müller, Stefan C / Ellinger, Jörg

Biochemical and biophysical research communications

2012 Volume 417, Issue 1, Page(s) 29–34

Abstract: Background: We investigated the role of the programmed cell death 4 (PDCD4) tumor suppressor gene in specimens of transitional cell carcinoma and of healthy individuals.: Methods: PDCD4 immunohistochemical expression was investigated in 294 cases in ... ...

Abstract	Background: We investigated the role of the programmed cell death 4 (PDCD4) tumor suppressor gene in specimens of transitional cell carcinoma and of healthy individuals. Methods: PDCD4 immunohistochemical expression was investigated in 294 cases in histologically proven transitional cell carcinoma in different tumorous stages (28 controls, 122 non-muscle invasive urothelial carcinoma, stages Tis-T1, 119 invasive transitional cell carcinoma stages T2-T4 and 25 metastases). MiR-21 expression, an important PDCD4 regulator, was assessed with real-time PCR analysis and showed inverse correlation to tissue PDCD4 expression. Results: Nuclear and cytoplasmatic PDCD4 immunostaining decreased significantly with histopathological progression of the tumor (p<0001). Controls showed strong nuclear and cytoplasmatic immunohistochemical staining. MiR-21 up regulation in tissue corresponded to PDCD4 suppression. Conclusions: These data support a decisive role for PDCD4 down regulation in transitional cell carcinoma and confirm miR-21 as a negative regulator for PDCD4. Additionally, PDCD4 immunohistochemical staining turns out to be a possible diagnostic marker for transitional cell carcinoma.
MeSH term(s)	Aged ; Aged, 80 and over ; Apoptosis Regulatory Proteins/biosynthesis ; Carcinoma, Transitional Cell/metabolism ; Carcinoma, Transitional Cell/pathology ; Female ; Humans ; Male ; MicroRNAs/biosynthesis ; Middle Aged ; Neoplasm Staging ; Prognosis ; RNA-Binding Proteins/biosynthesis ; Urologic Neoplasms/metabolism ; Urologic Neoplasms/pathology ; Urothelium/metabolism ; Urothelium/pathology
Chemical Substances	Apoptosis Regulatory Proteins ; MIRN21 microRNA, human ; MicroRNAs ; PDCD4 protein, human ; RNA-Binding Proteins
Language	English
Publishing date	2012-01-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2011.11.035
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