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Article ; Online: Primary Cilium Is Involved in Stem Cell Differentiation and Renewal through the Regulation of Multiple Signaling Pathways.

Yanardag, Sila / Pugacheva, Elena N

2021 Volume 10, Issue 6

Abstract: Signaling networks guide stem cells during their lineage specification and terminal differentiation. Primary cilium, an antenna-like protrusion, directly or indirectly plays a significant role in this guidance. All stem cells characterized so far have ... ...

Abstract	Signaling networks guide stem cells during their lineage specification and terminal differentiation. Primary cilium, an antenna-like protrusion, directly or indirectly plays a significant role in this guidance. All stem cells characterized so far have primary cilia. They serve as entry- or check-points for various signaling events by controlling the signal transduction and stability. Thus, defects in the primary cilia formation or dynamics cause developmental and health problems, including but not limited to obesity, cardiovascular and renal anomalies, hearing and vision loss, and even cancers. In this review, we focus on the recent findings of how primary cilium controls various signaling pathways during stem cell differentiation and identify potential gaps in the field for future research.
MeSH term(s)	Animals ; Cell Differentiation ; Cell Proliferation ; Cilia/metabolism ; Humans ; Signal Transduction ; Stem Cells/cytology
Language	English
Publishing date	2021-06-08
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10061428
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Primary Cilium Is Involved in Stem Cell Differentiation and Renewal through the Regulation of Multiple Signaling Pathways

Sila Yanardag / Elena N. Pugacheva

Cells, Vol 10, Iss 1428, p

2021 Volume 1428

Abstract	Signaling networks guide stem cells during their lineage specification and terminal differentiation. Primary cilium, an antenna-like protrusion, directly or indirectly plays a significant role in this guidance. All stem cells characterized so far have primary cilia. They serve as entry- or check-points for various signaling events by controlling the signal transduction and stability. Thus, defects in the primary cilia formation or dynamics cause developmental and health problems, including but not limited to obesity, cardiovascular and renal anomalies, hearing and vision loss, and even cancers. In this review, we focus on the recent findings of how primary cilium controls various signaling pathways during stem cell differentiation and identify potential gaps in the field for future research.
Keywords	primary cilia ; stem cells ; cancer stem cells ; signaling ; differentiation ; Notch ; Biology (General) ; QH301-705.5
Subject code	571
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Targeting primary cilia - associated signaling in glioblastoma: guided approach for drug development.

Loskutov, Yuriy / Pugacheva, Elena N

Oncoscience

2019 Volume 6, Issue 1-2, Page(s) 289–290

Language	English
Publishing date	2019-01-31
Publishing country	United States
Document type	Journal Article
ISSN	2331-4737
ISSN	2331-4737
DOI	10.18632/oncoscience.475
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Article: NEDD9 Overexpression Causes Hyperproliferation of Luminal Cells and Cooperates with HER2 Oncogene in Tumor Initiation: A Novel Prognostic Marker in Breast Cancer.

Purazo, Marc L / Ice, Ryan J / Shimpi, Rahul / Hoenerhoff, Mark / Pugacheva, Elena N

Cancers

2023 Volume 15, Issue 4

Abstract: HER2 overexpression occurs in 10-20% of breast cancer patients. HER2+ tumors are characterized by an increase in Ki67, early relapse, and increased metastasis. Little is known about the factors influencing early stages of HER2- tumorigenesis and ... ...

Abstract	HER2 overexpression occurs in 10-20% of breast cancer patients. HER2+ tumors are characterized by an increase in Ki67, early relapse, and increased metastasis. Little is known about the factors influencing early stages of HER2- tumorigenesis and diagnostic markers. Previously, it was shown that the deletion of NEDD9 in mouse models of HER2 cancer interferes with tumor growth, but the role of NEDD9 upregulation is currently unexplored. We report that NEDD9 is overexpressed in a significant subset of HER2+ breast cancers and correlates with a limited response to anti-HER2 therapy. To investigate the mechanisms through which NEDD9 influences HER2-dependent tumorigenesis, we generated MMTV-Cre-NEDD9 transgenic mice. The analysis of mammary glands shows extensive ductal epithelium hyperplasia, increased branching, and terminal end bud expansion. The addition of oncogene Erbb2 (neu) leads to the earlier development of early hyperplastic benign lesions (~16 weeks), with a significantly shorter latency than the control mice. Similarly, NEDD9 upregulation in MCF10A-derived acini leads to hyperplasia-like DCIS. This phenotype is associated with activation of ERK1/2 and AURKA kinases, leading to an increased proliferation of luminal cells. These findings indicate that NEDD9 is setting permissive conditions for HER2-induced tumorigenesis, thus identifying this protein as a potential diagnostic marker for early detection.
Language	English
Publishing date	2023-02-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers15041119
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Article ; Online: Expression-Based Diagnosis, Treatment Selection, and Drug Development for Breast Cancer.

Ye, Qing / Wang, Jiajia / Ducatman, Barbara / Raese, Rebecca A / Rogers, Jillian L / Wan, Ying-Wooi / Dong, Chunlin / Padden, Lindsay / Pugacheva, Elena N / Qian, Yong / Guo, Nancy Lan

International journal of molecular sciences

2023 Volume 24, Issue 13

Abstract: There is currently no gene expression assay that can assess if premalignant lesions will develop into invasive breast cancer. This study sought to identify biomarkers for selecting patients with a high potential for developing invasive carcinoma in the ... ...

Abstract	There is currently no gene expression assay that can assess if premalignant lesions will develop into invasive breast cancer. This study sought to identify biomarkers for selecting patients with a high potential for developing invasive carcinoma in the breast with normal histology, benign lesions, or premalignant lesions. A set of 26-gene mRNA expression profiles were used to identify invasive ductal carcinomas from histologically normal tissue and benign lesions and to select those with a higher potential for future cancer development (ADHC) in the breast associated with atypical ductal hyperplasia (ADH). The expression-defined model achieved an overall accuracy of 94.05% (AUC = 0.96) in classifying invasive ductal carcinomas from histologically normal tissue and benign lesions (
MeSH term(s)	Humans ; Female ; Breast Neoplasms/diagnosis ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Carcinoma, Ductal, Breast/diagnosis ; Carcinoma, Ductal, Breast/drug therapy ; Carcinoma, Ductal, Breast/genetics ; Patient Selection ; Hyperplasia/pathology ; Breast/metabolism ; Carcinoma, Intraductal, Noninfiltrating/pathology ; Drug Development ; Proto-Oncogene Proteins ; Homeodomain Proteins
Chemical Substances	PBX2 protein, human ; Proto-Oncogene Proteins ; Homeodomain Proteins
Language	English
Publishing date	2023-06-23
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241310561
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Article ; Online: Expression-Based Diagnosis, Treatment Selection, and Drug Development for Breast Cancer

Qing Ye / Jiajia Wang / Barbara Ducatman / Rebecca A. Raese / Jillian L. Rogers / Ying-Wooi Wan / Chunlin Dong / Lindsay Padden / Elena N. Pugacheva / Yong Qian / Nancy Lan Guo

International Journal of Molecular Sciences, Vol 24, Iss 10561, p

2023 Volume 10561

Abstract: ... ductal carcinomas from histologically normal tissue and benign lesions ( n = 185). This gene signature classified ... cancer development in ADH tissues with an overall accuracy of 100% ( n = 8). The mRNA expression patterns ... of these 26 genes were validated using RT-PCR analyses of independent tissue samples ( n = 77) and ...

Abstract	There is currently no gene expression assay that can assess if premalignant lesions will develop into invasive breast cancer. This study sought to identify biomarkers for selecting patients with a high potential for developing invasive carcinoma in the breast with normal histology, benign lesions, or premalignant lesions. A set of 26-gene mRNA expression profiles were used to identify invasive ductal carcinomas from histologically normal tissue and benign lesions and to select those with a higher potential for future cancer development (ADHC) in the breast associated with atypical ductal hyperplasia (ADH). The expression-defined model achieved an overall accuracy of 94.05% (AUC = 0.96) in classifying invasive ductal carcinomas from histologically normal tissue and benign lesions ( n = 185). This gene signature classified cancer development in ADH tissues with an overall accuracy of 100% ( n = 8). The mRNA expression patterns of these 26 genes were validated using RT-PCR analyses of independent tissue samples ( n = 77) and blood samples ( n = 48). The protein expression of PBX2 and RAD52 assessed with immunohistochemistry were prognostic of breast cancer survival outcomes. This signature provided significant prognostic stratification in The Cancer Genome Atlas breast cancer patients ( n = 1100), as well as basal-like and luminal A subtypes, and was associated with distinct immune infiltration and activities. The mRNA and protein expression of the 26 genes was associated with sensitivity or resistance to 18 NCCN-recommended drugs for treating breast cancer. Eleven genes had significant proliferative potential in CRISPR-Cas9/RNAi screening. Based on this gene expression signature, the VEGFR inhibitor ZM-306416 was discovered as a new drug for treating breast cancer.
Keywords	atypical ductal hyperplasia (ADH) ; atypical ductal hyperplasia with cancer (ADHC) ; diagnosis ; CRISPR-Cas9/RNAi ; immunohistochemistry ; triple-negative breast cancer (TNBC) ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	616 ; 610
Language	English
Publishing date	2023-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Skeletal muscle reprogramming by breast cancer regardless of treatment history or tumor molecular subtype.

Wilson, Hannah E / Stanton, David A / Montgomery, Cortney / Infante, Aniello M / Taylor, Matthew / Hazard-Jenkins, Hannah / Pugacheva, Elena N / Pistilli, Emidio E

NPJ breast cancer

2020 Volume 6, Page(s) 18

Abstract: Increased susceptibility to fatigue is a negative predictor of survival commonly experienced by women with breast cancer (BC). Here, we sought to identify molecular changes induced in human skeletal muscle by BC regardless of treatment history or tumor ... ...

Abstract	Increased susceptibility to fatigue is a negative predictor of survival commonly experienced by women with breast cancer (BC). Here, we sought to identify molecular changes induced in human skeletal muscle by BC regardless of treatment history or tumor molecular subtype using RNA-sequencing (RNA-seq) and proteomic analyses. Mitochondrial dysfunction was apparent across all molecular subtypes, with the greatest degree of transcriptomic changes occurring in women with HER2/neu-overexpressing tumors, though muscle from patients of all subtypes exhibited similar pathway-level dysregulation. Interestingly, we found no relationship between anticancer treatments and muscle gene expression, suggesting that fatigue is a product of BC per se rather than clinical history. In vitro and in vivo experimentation confirmed the ability of BC cells to alter mitochondrial function and ATP content in muscle. These data suggest that interventions supporting muscle in the presence of BC-induced mitochondrial dysfunction may alleviate fatigue and improve the lives of women with BC.
Language	English
Publishing date	2020-06-04
Publishing country	United States
Document type	Journal Article
ISSN	2374-4677
ISSN	2374-4677
DOI	10.1038/s41523-020-0162-2
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Article ; Online: Functional Hierarchy and Cooperation of EMT Master Transcription Factors in Breast Cancer Metastasis.

Addison, Joseph B / Voronkova, Maria A / Fugett, James H / Lin, Chen-Chung / Linville, Nathaniel C / Trinh, Brandon / Livengood, Ryan H / Smolkin, Matthew B / Schaller, Michael D / Ruppert, J Michael / Pugacheva, Elena N / Creighton, Chad J / Ivanov, Alexey V

Molecular cancer research : MCR

2021 Volume 19, Issue 5, Page(s) 784–798

Abstract: Several master transcription factors (TF) can activate the epithelial-to-mesenchymal transition (EMT). However, their individual and combinatorial contributions to EMT in breast cancer are not defined. We show that overexpression of EMT-TFs individually ... ...

Abstract	Several master transcription factors (TF) can activate the epithelial-to-mesenchymal transition (EMT). However, their individual and combinatorial contributions to EMT in breast cancer are not defined. We show that overexpression of EMT-TFs individually in epithelial cells upregulated endogenous SNAI2, ZEB1/2, TCF4, and TWIST1/2 as a result of positive feedback mediated in part by suppression of their negative regulator miRNAs miR200s/203/205. We identified TCF4 as a potential new target of miR200s. Expression of ZEB1/2 strongly correlated with the mesenchymal phenotype in breast cancer cells, with the CD24
MeSH term(s)	Animals ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Culture Techniques ; Cell Line, Tumor ; Cell Proliferation/physiology ; Epithelial-Mesenchymal Transition ; Female ; Heterografts ; Humans ; Male ; Mice ; Mice, Inbred NOD ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Neoplasm Metastasis ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Zinc Finger E-box Binding Homeobox 2/genetics ; Zinc Finger E-box Binding Homeobox 2/metabolism ; Zinc Finger E-box-Binding Homeobox 1/genetics ; Zinc Finger E-box-Binding Homeobox 1/metabolism
Chemical Substances	MicroRNAs ; Transcription Factors ; ZEB1 protein, human ; ZEB2 protein, human ; Zinc Finger E-box Binding Homeobox 2 ; Zinc Finger E-box-Binding Homeobox 1
Language	English
Publishing date	2021-01-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-20-0532
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Zs.A 5744: Show issues

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bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Nuclear Aurora-A kinase-induced hypoxia signaling drives early dissemination and metastasis in breast cancer: implications for detection of metastatic tumors.

Whately, Kristina M / Voronkova, Maria A / Maskey, Abha / Gandhi, Jasleen / Loskutov, Juergen / Choi, Hyeran / Yanardag, Sila / Chen, Dongquan / Wen, Sijin / Margaryan, Naira V / Smolkin, Matthew B / Purazo, Marc L / Hu, Gangqing / Pugacheva, Elena N

Oncogene

2021 Volume 40, Issue 37, Page(s) 5651–5664

Abstract: ... the expression of multiple HIF-dependent genes induced by nuclear AURKA (N-AURKA), including migration/invasion ... revealed a correlation between N-AURKA presence and decreased patient survival. Our results establish ...

Abstract	Metastatic breast cancer causes most breast cancer-associated deaths, especially in triple negative breast cancers (TNBC). The metastatic drivers of TNBCs are still poorly understood, and effective treatment non-existent. Here we reveal that the presence of Aurora-A Kinase (AURKA) in the nucleus and metastatic dissemination are molecularly connected through HIF1 (Hypoxia-Inducible Factor-1) signaling. Nuclear AURKA activates transcription of "hypoxia-induced genes" under normoxic conditions (pseudohypoxia) and without upregulation of oxygen-sensitive HIF1A subunit. We uncover that AURKA preferentially binds to HIF1B and co-localizes with the HIF complex on DNA. The mass-spectrometry analysis of the AURKA complex further confirmed the presence of CBP and p300 along with other TFIIB/RNApol II components. Importantly, the expression of multiple HIF-dependent genes induced by nuclear AURKA (N-AURKA), including migration/invasion, survival/death, and stemness, promote early cancer dissemination. These results indicate that nuclear, but not cytoplasmic, AURKA is a novel driver of early metastasis. Analysis of clinical tumor specimens revealed a correlation between N-AURKA presence and decreased patient survival. Our results establish a mechanistic link between two critical pathways in cancer metastasis, identifying nuclear AURKA as a crucial upstream regulator of the HIF1 transcription complex and a target for anti-metastatic therapy.
MeSH term(s)	Aurora Kinase A ; Cell Communication ; Cell Nucleus ; E1A-Associated p300 Protein ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; Signal Transduction ; Triple Negative Breast Neoplasms
Chemical Substances	HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; E1A-Associated p300 Protein (EC 2.3.1.48) ; EP300 protein, human (EC 2.3.1.48) ; Aurora Kinase A (EC 2.7.11.1)
Language	English
Publishing date	2021-07-29
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-021-01969-1
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Zs.A 2218: 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 ; Online: LPA signaling is regulated through the primary cilium: a novel target in glioblastoma.

Loskutov, Yuriy V / Griffin, Caryn L / Marinak, Kristina M / Bobko, Andrey / Margaryan, Naira V / Geldenhuys, Werner J / Sarkaria, Jann N / Pugacheva, Elena N

Oncogene

2018 Volume 37, Issue 11, Page(s) 1457–1471

Abstract: The primary cilium is a ubiquitous organelle presented on most human cells. It is a crucial signaling hub for multiple pathways including growth factor and G-protein coupled receptors. Loss of primary cilia, observed in various cancers, has been shown to ...

Abstract	The primary cilium is a ubiquitous organelle presented on most human cells. It is a crucial signaling hub for multiple pathways including growth factor and G-protein coupled receptors. Loss of primary cilia, observed in various cancers, has been shown to affect cell proliferation. Primary cilia formation is drastically decreased in glioblastoma (GBM), however, the role of cilia in normal astrocyte or glioblastoma proliferation has not been explored. Here, we report that loss of primary cilia in human astrocytes stimulates growth rate in a lysophosphatidic acid (LPA)-dependent manner. We show that lysophosphatidic acid receptor 1 (LPAR1) is accumulated in primary cilia. LPAR1 signaling through Gα12/Gαq was previously reported to be responsible for cancer cell proliferation. We found that in ciliated cells, Gα12 and Gαq are excluded from the cilium, creating a barrier against unlimited proliferation, one of the hallmarks of cancer. Upon loss of primary cilia, LPAR1 redistributes to the plasma membrane with a concomitant increase in LPAR1 association with Gα12 and Gαq. Inhibition of LPA signaling with the small molecule compound Ki16425 in deciliated highly proliferative astrocytes or glioblastoma patient-derived cells/xenografts drastically suppresses their growth both in vitro and in vivo. Moreover, Ki16425 brain delivery via PEG-PLGA nanoparticles inhibited tumor progression in an intracranial glioblastoma PDX model. Overall, our findings establish a novel mechanism by which primary cilium restricts proliferation and indicate that loss of primary cilia is sufficient to increase mitogenic signaling, and is important for the maintenance of a highly proliferative phenotype. Clinical application of LPA inhibitors may prove beneficial to restrict glioblastoma growth and ensure local control of disease.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Astrocytes/drug effects ; Astrocytes/metabolism ; Astrocytes/ultrastructure ; Brain Neoplasms/drug therapy ; Brain Neoplasms/metabolism ; Brain Neoplasms/pathology ; Cell Proliferation/drug effects ; Cilia/drug effects ; Cilia/pathology ; Cilia/physiology ; Glioblastoma/drug therapy ; Glioblastoma/metabolism ; Glioblastoma/pathology ; Humans ; Lysophospholipids/antagonists & inhibitors ; Lysophospholipids/metabolism ; Lysophospholipids/pharmacology ; Male ; Mice ; Mice, Inbred NOD ; Mice, Transgenic ; Molecular Targeted Therapy ; Receptors, Lysophosphatidic Acid/antagonists & inhibitors ; Receptors, Lysophosphatidic Acid/genetics ; Receptors, Lysophosphatidic Acid/metabolism ; Signal Transduction/drug effects ; Xenograft Model Antitumor Assays
Chemical Substances	Antineoplastic Agents ; LPAR1 protein, human ; Lysophospholipids ; Receptors, Lysophosphatidic Acid ; lysophosphatidic acid (PG6M3969SG)
Language	English
Publishing date	2018-01-11
Publishing country	England
Document type	Journal Article
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-017-0049-3
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Zs.A 2218: Show issues

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