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Article ; Online: Activation of HIF-1

Schoos, Alexandra / Gabriel, Cordula / Knab, Vanessa M / Fux, Daniela A

The Journal of pharmacology and experimental therapeutics

2019 Volume 370, Issue 3, Page(s) 480–489

Abstract: Opioids promote tumor angiogenesis in mammary malignancies, but the underlying signaling mechanism is largely unknown. The current study investigated the hypothesis that stimulation ... ...

Abstract	Opioids promote tumor angiogenesis in mammary malignancies, but the underlying signaling mechanism is largely unknown. The current study investigated the hypothesis that stimulation of
MeSH term(s)	Breast Neoplasms/pathology ; Cyclooxygenase 2/metabolism ; Dinoprostone/metabolism ; Endothelial Cells/metabolism ; Enkephalin, Leucine-2-Alanine/pharmacology ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; MCF-7 Cells ; Paracrine Communication/drug effects ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphoinositide-3 Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins c-akt/antagonists & inhibitors ; Receptors, sigma/agonists ; Receptors, sigma/metabolism ; Signal Transduction/drug effects ; Vascular Endothelial Growth Factor A/metabolism
Chemical Substances	HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; Phosphoinositide-3 Kinase Inhibitors ; Receptors, sigma ; Vascular Endothelial Growth Factor A ; Enkephalin, Leucine-2-Alanine (63631-40-3) ; Cyclooxygenase 2 (EC 1.14.99.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2019-07-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	3106-9
ISSN	1521-0103 ; 0022-3565
ISSN (online)	1521-0103
ISSN	0022-3565
DOI	10.1124/jpet.119.257501
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Article: CDK6 Degradation Is Counteracted by p16

Schmalzbauer, Belinda S / Thondanpallil, Teresemary / Heller, Gerwin / Schirripa, Alessia / Sperl, Clio-Melina / Mayer, Isabella M / Knab, Vanessa M / Nebenfuehr, Sofie / Zojer, Markus / Mueller, André C / Fontaine, Frédéric / Klampfl, Thorsten / Sexl, Veronika / Kollmann, Karoline

Cancers

2022 Volume 14, Issue 6

Abstract: Cyclin-dependent kinase 6 (CDK6) represents a novel therapeutic target for the treatment of certain subtypes of acute myeloid leukaemia (AML). CDK4/6 kinase inhibitors have been widely studied in many cancer types and their effects may be limited by ... ...

Abstract	Cyclin-dependent kinase 6 (CDK6) represents a novel therapeutic target for the treatment of certain subtypes of acute myeloid leukaemia (AML). CDK4/6 kinase inhibitors have been widely studied in many cancer types and their effects may be limited by primary and secondary resistance mechanisms. CDK4/6 degraders, which eliminate kinase-dependent and kinase-independent effects, have been suggested as an alternative therapeutic option. We show that the efficacy of the CDK6-specific protein degrader BSJ-03-123 varies among AML subtypes and depends on the low expression of the INK4 proteins p16
Language	English
Publishing date	2022-03-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14061554
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Article ; Online: Opioids drive breast cancer metastasis through the δ-opioid receptor and oncogenic STAT3.

Tripolt, Sabrina / Neubauer, Heidi A / Knab, Vanessa M / Elmer, Dominik P / Aberger, Fritz / Moriggl, Richard / Fux, Daniela A

Neoplasia (New York, N.Y.)

2021 Volume 23, Issue 2, Page(s) 270–279

Abstract: The opioid crisis of pain medication bears risks from addiction to cancer progression, but little experimental evidence exists. Expression of δ-opioid receptors (DORs) correlates with poor prognosis for breast cancer patients, but mechanistic insights ... ...

Abstract	The opioid crisis of pain medication bears risks from addiction to cancer progression, but little experimental evidence exists. Expression of δ-opioid receptors (DORs) correlates with poor prognosis for breast cancer patients, but mechanistic insights into oncogenic signaling mechanisms of opioid-triggered cancer progression are lacking. We show that orthotopic transplant models using human or murine breast cancer cells displayed enhanced metastasis upon opioid-induced DOR stimulation. Interestingly, opioid-exposed breast cancer cells showed enhanced migration and strong STAT3 activation, which was efficiently blocked by a DOR-antagonist. Furthermore, opioid treatment resulted in down-regulation of E-Cadherin and increased expression of epithelial-mesenchymal transition markers. Notably, STAT3 knockdown or upstream inhibition through the JAK1/2 kinase inhibitor ruxolitinib prevented opioid-induced breast cancer cell metastasis and migration in vitro and in vivo. We conclude on a novel mechanism whereby opioid-triggered breast cancer metastasis occurs via oncogenic JAK1/2-STAT3 signaling to promote epithelial-mesenchymal transition. These findings emphasize the importance of selective and restricted opioid use, as well as the need for safer pain medication that does not activate these oncogenic pathways.
MeSH term(s)	Analgesics, Opioid/pharmacology ; Animals ; Biomarkers ; Breast Neoplasms/etiology ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Disease Models, Animal ; Disease Susceptibility ; Female ; Gene Expression ; Humans ; Immunohistochemistry ; Mice ; Mice, Transgenic ; Neoplasm Metastasis ; Oncogene Proteins/metabolism ; Receptors, Opioid, delta/agonists ; Receptors, Opioid, delta/genetics ; Receptors, Opioid, delta/metabolism ; STAT3 Transcription Factor/metabolism
Chemical Substances	Analgesics, Opioid ; Biomarkers ; Oncogene Proteins ; Receptors, Opioid, delta ; STAT3 Transcription Factor
Language	English
Publishing date	2021-01-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1483840-0
ISSN	1476-5586 ; 1522-8002
ISSN (online)	1476-5586
ISSN	1522-8002
DOI	10.1016/j.neo.2020.12.011
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Article ; Online: In vitro study to assess the efficacy of CDK4/6 inhibitor Palbociclib (PD-0332991) for treating canine mammary tumours.

Schoos, Alexandra / Knab, Vanessa M / Gabriel, Cordula / Tripolt, Sabrina / Wagner, Daniela A / Bauder, Barbara / Url, Angelika / Fux, Daniela A

Veterinary and comparative oncology

2019 Volume 17, Issue 4, Page(s) 507–521

Abstract: Therapy of canine mammary tumours (CMTs) with classical antitumour drugs is problematic, so better therapeutic options are needed. Palbociclib (PD-0332991) is an innovative and effective anticancer drug for the treatment of breast cancer in women. ... ...

Abstract	Therapy of canine mammary tumours (CMTs) with classical antitumour drugs is problematic, so better therapeutic options are needed. Palbociclib (PD-0332991) is an innovative and effective anticancer drug for the treatment of breast cancer in women. Palbociclib is an inhibitor of cyclin-dependent kinase 4 (CDK4) and CDK6, which are key regulators of the cell cycle machinery and thus cell proliferation. In the present in vitro study, we investigated whether Palbociclib also represents a candidate drug to combat CMT. For this purpose, the effect of Palbociclib was analysed in P114 and CF41 cells, two CMT cell lines with an endogenous CDK4/6 co-expression. Incubation of P114 and CF41 cells with Palbociclib resulted in a dose- and time-dependent loss of phosphorylated retinoblastoma protein (pRb), a classical CDK4/6 substrate within the cell cycle machinery. Moreover, treatment of CMT cells with Palbociclib-induced cell cycle arrest affected cell viability, prevented colony formation and impaired cell migration activity. Palbociclib also inhibited the growth of P114 and CF41 cell spheroids. Immunohistochemical analysis of canine patient samples revealed a consistent expression of CDK6 in different canine mammary carcinoma types, but an individual and tumour-specific expression pattern of phosphorylated pRb independent of the tumour grade. Together, our findings let us suggest that Palbociclib has antitumour effects on CMT cells and that canine patients may represent potential candidates for treatment with this CDK4/6 inhibitor.
MeSH term(s)	Adenocarcinoma/drug therapy ; Animals ; Antineoplastic Agents/therapeutic use ; Cell Line, Tumor ; Cell Movement ; Cyclin-Dependent Kinase 4/antagonists & inhibitors ; Cyclin-Dependent Kinase 6/antagonists & inhibitors ; Dog Diseases/drug therapy ; Dogs ; Female ; Mammary Neoplasms, Animal/drug therapy ; Piperazines/therapeutic use ; Pyridines/therapeutic use
Chemical Substances	Antineoplastic Agents ; Piperazines ; Pyridines ; Cyclin-Dependent Kinase 4 (EC 2.7.11.22) ; Cyclin-Dependent Kinase 6 (EC 2.7.11.22) ; palbociclib (G9ZF61LE7G)
Language	English
Publishing date	2019-07-12
Publishing country	England
Document type	Journal Article
ZDB-ID	2129634-0
ISSN	1476-5829 ; 1476-5810
ISSN (online)	1476-5829
ISSN	1476-5810
DOI	10.1111/vco.12514
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Article ; Online: A STAT5B-CD9 axis determines self-renewal in hematopoietic and leukemic stem cells.

Kollmann, Sebastian / Grausenburger, Reinhard / Klampfl, Thorsten / Prchal-Murphy, Michaela / Bastl, Klavdija / Pisa, Hanja / Knab, Vanessa M / Brandstoetter, Tania / Doma, Eszter / Sperr, Wolfgang R / Lagger, Sabine / Farlik, Matthias / Moriggl, Richard / Valent, Peter / Halbritter, Florian / Kollmann, Karoline / Heller, Gerwin / Maurer, Barbara / Sexl, Veronika

Blood

2021 Volume 138, Issue 23, Page(s) 2347–2359

Abstract: The transcription factors signal transducer and activator of transcription 5A (STAT5A) and STAT5B are critical in hematopoiesis and leukemia. They are widely believed to have redundant functions, but we describe a unique role for STAT5B in driving the ... ...

Abstract	The transcription factors signal transducer and activator of transcription 5A (STAT5A) and STAT5B are critical in hematopoiesis and leukemia. They are widely believed to have redundant functions, but we describe a unique role for STAT5B in driving the self-renewal of hematopoietic and leukemic stem cells (HSCs/LSCs). We find STAT5B to be specifically activated in HSCs and LSCs, where it induces many genes associated with quiescence and self-renewal, including the surface marker CD9. Levels of CD9 represent a prognostic marker for patients with STAT5-driven leukemia, and our findings suggest that anti-CD9 antibodies may be useful in their treatment to target and eliminate LSCs. We show that it is vital to consider STAT5A and STAT5B as distinct entities in normal and malignant hematopoiesis.
MeSH term(s)	Animals ; Cell Self Renewal ; Hematopoiesis ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/metabolism ; Hematopoietic Stem Cells/pathology ; Humans ; Leukemia/metabolism ; Leukemia/pathology ; Mice ; Mice, Inbred C57BL ; Neoplastic Stem Cells/cytology ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; STAT5 Transcription Factor/metabolism ; Signal Transduction ; Tetraspanin 29/metabolism ; Tumor Cells, Cultured
Chemical Substances	STAT5 Transcription Factor ; Tetraspanin 29
Language	English
Publishing date	2021-07-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2021010980
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Zs.MO 364: Show issues

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Article ; Online: Loss of NKG2D in murine NK cells leads to increased perforin production upon long-term stimulation with IL-2.

Prinz, Daniela / Klein, Klara / List, Julia / Knab, Vanessa M / Menzl, Ingeborg / Leidenfrost, Nicoletta / Heller, Gerwin / Polić, Bojan / Putz, Eva Maria / Witalisz-Siepracka, Agnieszka / Sexl, Veronika / Gotthardt, Dagmar

European journal of immunology

2020 Volume 50, Issue 6, Page(s) 880–890

Abstract: NK cells are innate lymphocytes responsible for lysis of pathogen-infected and transformed cells. One of the major activating receptors required for target cell recognition is the NK group 2D (NKG2D) receptor. Numerous reports show the necessity of NKG2D ...

Abstract	NK cells are innate lymphocytes responsible for lysis of pathogen-infected and transformed cells. One of the major activating receptors required for target cell recognition is the NK group 2D (NKG2D) receptor. Numerous reports show the necessity of NKG2D for effective tumor immune surveillance. Further studies identified NKG2D as a key element allowing tumor immune escape. We here use a mouse model with restricted deletion of NKG2D in mature NKp46
MeSH term(s)	Animals ; Cell Line, Tumor ; Immunity, Cellular/drug effects ; Immunity, Cellular/genetics ; Interferon-gamma/genetics ; Interferon-gamma/immunology ; Interleukin-2/pharmacology ; Killer Cells, Natural/immunology ; Killer Cells, Natural/pathology ; Mice ; Mice, Knockout ; NK Cell Lectin-Like Receptor Subfamily K/genetics ; NK Cell Lectin-Like Receptor Subfamily K/immunology ; Pore Forming Cytotoxic Proteins/genetics ; Pore Forming Cytotoxic Proteins/immunology
Chemical Substances	IFNG protein, mouse ; Interleukin-2 ; Klrk1 protein, mouse ; NK Cell Lectin-Like Receptor Subfamily K ; Pore Forming Cytotoxic Proteins ; perforin, mouse ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2020-02-20
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.201948222
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Zs.A 489: 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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Article: In vitro study to assess the efficacy of CDK4/6 inhibitor Palbociclib (PD‐0332991) for treating canine mammary tumours

Schoos, Alexandra / Knab, Vanessa M / Gabriel, Cordula / Tripolt, Sabrina / Wagner, Daniela A / Bauder, Barbara / Url, Angelika / Fux, Daniela A

Veterinary and comparative oncology. 2019 Dec., v. 17, no. 4

2019

Abstract: Therapy of canine mammary tumours (CMTs) with classical antitumour drugs is problematic, so better therapeutic options are needed. Palbociclib (PD‐0332991) is an innovative and effective anticancer drug for the treatment of breast cancer in women. ... ...

Abstract	Therapy of canine mammary tumours (CMTs) with classical antitumour drugs is problematic, so better therapeutic options are needed. Palbociclib (PD‐0332991) is an innovative and effective anticancer drug for the treatment of breast cancer in women. Palbociclib is an inhibitor of cyclin‐dependent kinase 4 (CDK4) and CDK6, which are key regulators of the cell cycle machinery and thus cell proliferation. In the present in vitro study, we investigated whether Palbociclib also represents a candidate drug to combat CMT. For this purpose, the effect of Palbociclib was analysed in P114 and CF41 cells, two CMT cell lines with an endogenous CDK4/6 co‐expression. Incubation of P114 and CF41 cells with Palbociclib resulted in a dose‐ and time‐dependent loss of phosphorylated retinoblastoma protein (pRb), a classical CDK4/6 substrate within the cell cycle machinery. Moreover, treatment of CMT cells with Palbociclib‐induced cell cycle arrest affected cell viability, prevented colony formation and impaired cell migration activity. Palbociclib also inhibited the growth of P114 and CF41 cell spheroids. Immunohistochemical analysis of canine patient samples revealed a consistent expression of CDK6 in different canine mammary carcinoma types, but an individual and tumour‐specific expression pattern of phosphorylated pRb independent of the tumour grade. Together, our findings let us suggest that Palbociclib has antitumour effects on CMT cells and that canine patients may represent potential candidates for treatment with this CDK4/6 inhibitor.
Keywords	antineoplastic agents ; breast neoplasms ; cell cycle checkpoints ; cell lines ; cell movement ; cell proliferation ; cell viability ; cyclin-dependent kinase ; dogs ; enzyme inhibitors ; immunohistochemistry ; in vitro studies ; mammary neoplasms (animal) ; patients ; therapeutics ; women
Language	English
Dates of publication	2019-12
Size	p. 507-521.
Publishing place	Blackwell Publishing Ltd
Document type	Article
Note	JOURNAL ARTICLE
ZDB-ID	2129634-0
ISSN	1476-5829 ; 1476-5810
ISSN (online)	1476-5829
ISSN	1476-5810
DOI	10.1111/vco.12514
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Acute Parathyroid Hormone Injection Increases C-Terminal but Not Intact Fibroblast Growth Factor 23 Levels.

Knab, Vanessa M / Corbin, Braden / Andrukhova, Olena / Hum, Julia M / Ni, Pu / Rabadi, Seham / Maeda, Akira / White, Kenneth E / Erben, Reinhold G / Jüppner, Harald / Christov, Marta

Endocrinology

2017 Volume 158, Issue 5, Page(s) 1130–1139

Abstract: The acute effects of parathyroid hormone (PTH) on fibroblast growth factor 23 (FGF23) in vivo are not well understood. After a single subcutaneous PTH (1-34) injection (50 nmol/kg) in mice, FGF23 levels were assessed in plasma using assays that measure ... ...

Abstract	The acute effects of parathyroid hormone (PTH) on fibroblast growth factor 23 (FGF23) in vivo are not well understood. After a single subcutaneous PTH (1-34) injection (50 nmol/kg) in mice, FGF23 levels were assessed in plasma using assays that measure either intact alone (iFGF23) or intact/C-terminal FGF23 (cFGF23). Furthermore, FGF23 messenger RNA (mRNA) and protein levels were assessed in bone. In addition, we examined the effects of PTH treatment on FGF23 production in vitro using differentiated calvarial osteocyte-like cells. cFGF23 levels increased by three- to fivefold within 2 hours following PTH injection, which returned to baseline by 4 hours. In contrast, iFGF23 levels remained unchanged for the first 2 hours, yet declined to ∼60% by 6 hours and remained suppressed before returning to baseline after 24 hours. Using homozygous mice for an autosomal dominant hypophosphatemic rickets-FGF23 mutation or animals treated with a furin inhibitor, we showed that cFGF23 and iFGF23 levels increased equivalently after PTH injection. These findings are consistent with increased FGF23 production in bone, yet rapid cleavage of the secreted intact protein. Using primary osteocyte-like cell cultures, we showed that PTH increased FGF23 mRNA expression through cyclic adenosine monophosphate/protein kinase A, but not inositol triphosphate/protein kinase C signaling; PTH also increased furin protein levels. In conclusion, PTH injection rapidly increases FGF23 production in bone in vivo and in vitro. However, iFGF23 is rapidly degraded. At later time points through an unidentified mechanism, a sustained decrease in FGF23 production occurs.
MeSH term(s)	Animals ; Bone and Bones/drug effects ; Bone and Bones/metabolism ; Cells, Cultured ; Female ; Fibroblast Growth Factors/blood ; Fibroblast Growth Factors/chemistry ; Fibroblast Growth Factors/metabolism ; Injections ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Osteocytes/drug effects ; Osteocytes/metabolism ; Parathyroid Hormone/administration & dosage ; Parathyroid Hormone/pharmacology ; Peptide Fragments/blood ; Protein Domains
Chemical Substances	Parathyroid Hormone ; Peptide Fragments ; fibroblast growth factor 23 ; Fibroblast Growth Factors (62031-54-3)
Language	English
Publishing date	2017-05-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2016-1451
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Article ; Online: A kinase-independent role for CDK8 in BCR-ABL1+ leukemia

Ingeborg Menzl / Tinghu Zhang / Angelika Berger-Becvar / Reinhard Grausenburger / Gerwin Heller / Michaela Prchal-Murphy / Leo Edlinger / Vanessa M. Knab / Iris Z. Uras / Eva Grundschober / Karin Bauer / Mareike Roth / Anna Skucha / Yao Liu / John M. Hatcher / Yanke Liang / Nicholas P. Kwiatkowski / Daniela Fux / Andrea Hoelbl-Kovacic /

Stefan Kubicek / Junia V. Melo / Peter Valent / Thomas Weichhart / Florian Grebien / Johannes Zuber / Nathanael S. Gray / Veronika Sexl

Nature Communications, Vol 10, Iss 1, Pp 1-

2019 Volume 15

Abstract: Cyclin-dependent kinases are deregulated in blood cancers. Here, the authors show that CDK8, independent of its kinase activity, regulates mTOR signalling for the maintenance of BCR-ABL1+ leukemia, and that the dual inhibition of CDK8 and mTOR signalling ...

Abstract	Cyclin-dependent kinases are deregulated in blood cancers. Here, the authors show that CDK8, independent of its kinase activity, regulates mTOR signalling for the maintenance of BCR-ABL1+ leukemia, and that the dual inhibition of CDK8 and mTOR signalling induces apoptosis in these cells.
Keywords	Science ; Q
Language	English
Publishing date	2019-10-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: A kinase-independent role for CDK8 in BCR-ABL1+ leukemia

Stefan Kubicek / Junia V. Melo / Peter Valent / Thomas Weichhart / Florian Grebien / Johannes Zuber / Nathanael S. Gray / Veronika Sexl

Nature Communications, Vol 10, Iss 1, Pp 1-

2019 Volume 15

Abstract	Cyclin-dependent kinases are deregulated in blood cancers. Here, the authors show that CDK8, independent of its kinase activity, regulates mTOR signalling for the maintenance of BCR-ABL1+ leukemia, and that the dual inhibition of CDK8 and mTOR signalling induces apoptosis in these cells.
Keywords	Science ; Q
Language	English
Publishing date	2019-10-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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