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Article ; Online: H2-gamendazole: a new therapeutic lead for the treatment of polycystic kidney disease.

Pirestani, Shabnam / Golemis, Erica A

American journal of physiology. Renal physiology

2022 Volume 323, Issue 6, Page(s) F613–F615

MeSH term(s)	Humans ; Polycystic Kidney Diseases/drug therapy ; Polycystic Kidney, Autosomal Dominant/drug therapy ; Indazoles/therapeutic use
Chemical Substances	gamendazole ; Indazoles
Language	English
Publishing date	2022-09-15
Publishing country	United States
Document type	Editorial
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00225.2022
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Uc I Zs.89: Show issues

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Article ; Online: Intrapancreatic fat, pancreatitis, and pancreatic cancer.

Lilly, Anna C / Astsaturov, Igor / Golemis, Erica A

Cellular and molecular life sciences : CMLS

2023 Volume 80, Issue 8, Page(s) 206

Abstract: Pancreatic cancer is typically detected at an advanced stage, and is refractory to most forms of treatment, contributing to poor survival outcomes. The incidence of pancreatic cancer is gradually increasing, linked to an aging population and increasing ... ...

Abstract	Pancreatic cancer is typically detected at an advanced stage, and is refractory to most forms of treatment, contributing to poor survival outcomes. The incidence of pancreatic cancer is gradually increasing, linked to an aging population and increasing rates of obesity and pancreatitis, which are risk factors for this cancer. Sources of risk include adipokine signaling from fat cells throughout the body, elevated levels of intrapancreatic intrapancreatic adipocytes (IPAs), inflammatory signals arising from pancreas-infiltrating immune cells and a fibrotic environment induced by recurring cycles of pancreatic obstruction and acinar cell lysis. Once cancers become established, reorganization of pancreatic tissue typically excludes IPAs from the tumor microenvironment, which instead consists of cancer cells embedded in a specialized microenvironment derived from cancer-associated fibroblasts (CAFs). While cancer cell interactions with CAFs and immune cells have been the topic of much investigation, mechanistic studies of the source and function of IPAs in the pre-cancerous niche are much less developed. Intriguingly, an extensive review of studies addressing the accumulation and activity of IPAs in the pancreas reveals that unexpectedly diverse group of factors cause replacement of acinar tissue with IPAs, particularly in the mouse models that are essential tools for research into pancreatic cancer. Genes implicated in regulation of IPA accumulation include KRAS, MYC, TGF-β, periostin, HNF1, and regulators of ductal ciliation and ER stress, among others. These findings emphasize the importance of studying pancreas-damaging factors in the pre-cancerous environment, and have significant implications for the interpretation of data from mouse models for pancreatic cancer.
MeSH term(s)	Mice ; Animals ; Pancreatic Neoplasms/pathology ; Pancreatitis/pathology ; Pancreas/pathology ; Acinar Cells/pathology ; Carcinoma, Pancreatic Ductal/pathology ; Tumor Microenvironment ; Pancreatic Neoplasms
Language	English
Publishing date	2023-07-15
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-023-04855-z
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Zs.A 195: Show issues

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Article ; Online: Synergy of EGFR and AURKA inhibitors in KRAS-mutated non-small cell lung cancers.

Bagnyukova, Tetyana / Egleston, Brian L / Pavlov, Valerii A / Serebriiskii, Ilya G / Golemis, Erica A / Borghaei, Hossein

Cancer research communications

2024

Abstract: The most common oncogenic driver mutations for non-small cell lung cancer (NSCLC) activate the epidermal growth factor receptor (EGFR) or KRAS. Clinical trials exploring treatments for EGFR- or KRAS-mutated (EGFRmut or KRASmut) cancers have focused on ... ...

Abstract	The most common oncogenic driver mutations for non-small cell lung cancer (NSCLC) activate the epidermal growth factor receptor (EGFR) or KRAS. Clinical trials exploring treatments for EGFR- or KRAS-mutated (EGFRmut or KRASmut) cancers have focused on small molecule inhibitors targeting the driver mutations. Typically, these inhibitors perform more effectively based on combination with either chemotherapies, or other targeted therapies. For EGFRmut NSCLC, a combination of inhibitors of EGFR and Aurora-A kinase (AURKA), an oncogene commonly overexpressed in solid tumors, has shown promising activity in clinical trials. Interestingly, a number of recent studies have indicated that EGFR activity supports overall viability of tumors lacking EGFR mutations, and AURKA expression is abundant in KRASmut cell lines. In this study, we have evaluated dual inhibition of EGFR and AURKA in KRASmut NSCLC models. These data demonstrate synergy between the EGFR inhibitor erlotinib and the AURKA inhibitor alisertib in reducing cell viability and clonogenic capacity in vitro, associated with reduced activity of EGFR pathway effectors, accumulation of enhanced aneuploid cell populations, and elevated cell death. Importantly, the erlotinib-alisertib combination also synergistically reduces xenograft growth in vivo. Analysis of signaling pathways demonstrated that the combination of erlotinib and alisertib was more effective than single agent treatments at reducing activity of EGFR and pathway effectors following either brief or extended administration of the drugs. In sum, this study indicates value of inhibiting EGFR in KRASmut NSCLC, and suggests the specific value of dual inhibition of AURKA and EGFR in these tumors.
Language	English
Publishing date	2024-04-19
Publishing country	United States
Document type	Journal Article
ISSN	2767-9764
ISSN (online)	2767-9764
DOI	10.1158/2767-9764.CRC-23-0482
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Article ; Online: Aurora Kinases as Therapeutic Targets in Head and Neck Cancer.

Nguyen, Theodore T / Silva, Flaviane N / Golemis, Erica A

Cancer journal (Sudbury, Mass.)

2022 Volume 28, Issue 5, Page(s) 387–400

Abstract: Abstract: The Aurora kinases (AURKA and AURKB) have attracted attention as therapeutic targets in head and neck squamous cell carcinomas. Aurora kinases were first defined as regulators of mitosis that localization to the centrosome (AURKA) and ... ...

Abstract	Abstract: The Aurora kinases (AURKA and AURKB) have attracted attention as therapeutic targets in head and neck squamous cell carcinomas. Aurora kinases were first defined as regulators of mitosis that localization to the centrosome (AURKA) and centromere (AURKB), governing formation of the mitotic spindle, chromatin condensation, activation of the core mitotic kinase CDK1, alignment of chromosomes at metaphase, and other processes. Subsequently, additional roles for Aurora kinases have been defined in other phases of cell cycle, including regulation of ciliary disassembly and DNA replication. In cancer, elevated expression and activity of Aurora kinases result in enhanced or neomorphic locations and functions that promote aggressive disease, including promotion of MYC expression, oncogenic signaling, stem cell identity, epithelial-mesenchymal transition, and drug resistance. Numerous Aurora-targeted inhibitors have been developed and are being assessed in preclinical and clinical trials, with the goal of improving head and neck squamous cell carcinoma treatment.
MeSH term(s)	Aurora Kinase A/genetics ; Aurora Kinase A/metabolism ; Chromatin ; Head and Neck Neoplasms/drug therapy ; Humans ; Squamous Cell Carcinoma of Head and Neck/drug therapy
Chemical Substances	Chromatin ; Aurora Kinase A (EC 2.7.11.1)
Language	English
Publishing date	2022-09-27
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2018400-1
ISSN	1540-336X ; 1528-9117 ; 1081-4442
ISSN (online)	1540-336X
ISSN	1528-9117 ; 1081-4442
DOI	10.1097/PPO.0000000000000614
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Zs.A 4470: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 163: Show issues

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Article ; Online: Informatics-guided drug repurposing for Autosomal Dominant Polycystic Kidney Disease (ADPKD).

Kiseleva, Anna A / Golemis, Erica A

EBioMedicine

2020 Volume 52, Page(s) 102628

MeSH term(s)	Disease Progression ; Drug Repositioning ; Humans ; Informatics ; Polycystic Kidney, Autosomal Dominant
Language	English
Publishing date	2020-01-22
Publishing country	Netherlands
Document type	Journal Article ; Comment
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2020.102628
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Article ; Online: Delineating the RAS Conformational Landscape.

Parker, Mitchell I / Meyer, Joshua E / Golemis, Erica A / Dunbrack, Roland L

Cancer research

2022 Volume 82, Issue 13, Page(s) 2485–2498

Abstract: Mutations in RAS isoforms (KRAS, NRAS, and HRAS) are among the most frequent oncogenic alterations in many cancers, making these proteins high priority therapeutic targets. Effectively targeting RAS isoforms requires an exact understanding of their ... ...

Abstract	Mutations in RAS isoforms (KRAS, NRAS, and HRAS) are among the most frequent oncogenic alterations in many cancers, making these proteins high priority therapeutic targets. Effectively targeting RAS isoforms requires an exact understanding of their active, inactive, and druggable conformations. However, there is no structural catalog of RAS conformations to guide therapeutic targeting or examining the structural impact of RAS mutations. Here we present an expanded classification of RAS conformations based on analyses of the catalytic switch 1 (SW1) and switch 2 (SW2) loops. From 721 human KRAS, NRAS, and HRAS structures available in the Protein Data Bank (206 RAS-protein cocomplexes, 190 inhibitor-bound, and 325 unbound, including 204 WT and 517 mutated structures), we created a broad conformational classification based on the spatial positions of Y32 in SW1 and Y71 in SW2. Clustering all well-modeled SW1 and SW2 loops using a density-based machine learning algorithm defined additional conformational subsets, some previously undescribed. Three SW1 conformations and nine SW2 conformations were identified, each associated with different nucleotide states (GTP-bound, nucleotide-free, and GDP-bound) and specific bound proteins or inhibitor sites. The GTP-bound SW1 conformation could be further subdivided on the basis of the hydrogen bond type made between Y32 and the GTP γ-phosphate. Further analysis clarified the catalytic impact of G12D and G12V mutations and the inhibitor chemistries that bind to each druggable RAS conformation. Overall, this study has expanded our understanding of RAS structural biology, which could facilitate future RAS drug discovery. Significance: Analysis of >700 RAS structures helps define an expanded landscape of active, inactive, and druggable RAS conformations, the structural impact of common RAS mutations, and previously uncharacterized RAS inhibitor-binding modes.
MeSH term(s)	Guanosine Triphosphate/metabolism ; Humans ; Mutation ; Protein Conformation ; Protein Isoforms/metabolism ; Proto-Oncogene Proteins p21(ras)/genetics ; Proto-Oncogene Proteins p21(ras)/metabolism ; ras Proteins/genetics ; ras Proteins/metabolism
Chemical Substances	Protein Isoforms ; Guanosine Triphosphate (86-01-1) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; ras Proteins (EC 3.6.5.2)
Language	English
Publishing date	2022-05-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-22-0804
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Article ; Online: Identification of the KRIT1 Protein by LexA-Based Yeast Two-Hybrid System.

Serebriiskii, Ilya G / Elmekawy, Mohamed / Golemis, Erica A

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

2020 Volume 2152, Page(s) 269–289

Abstract: Cerebral cavernous malformation (CCM) is a vascular malformation of the central nervous system that is associated with leaky capillaries, and a predisposition to serious clinical conditions including intracerebral hemorrhage and seizures. Germline or ... ...

Abstract	Cerebral cavernous malformation (CCM) is a vascular malformation of the central nervous system that is associated with leaky capillaries, and a predisposition to serious clinical conditions including intracerebral hemorrhage and seizures. Germline or sporadic mutations in the CCM1/KRIT1 gene are responsible for the majority of cases of CCM. In this article, we describe the original characterization of the CCM1/KRIT1 gene. This cloning was done through the use of a variant of the yeast two-hybrid screen known as the interaction trap, using the RAS-family GTPase KREV1/RAP1A as a bait. The partial clone of KRIT1 (Krev1 Interaction Trapped) initially identified was extended through 5'RACE and computational analysis to obtain a full-length cDNA, then used in a sequential screen to define the integrin-associated ICAP1 protein as a KRIT1 partner protein. We discuss how these interactions are relevant to the current understanding of KRIT1/CCM1 biology, and provide a protocol for library screening with the Interaction Trap.
MeSH term(s)	Genetic Association Studies/methods ; Genotype ; Hemangioma, Cavernous, Central Nervous System/genetics ; Hemangioma, Cavernous, Central Nervous System/metabolism ; Humans ; KRIT1 Protein/genetics ; KRIT1 Protein/metabolism ; Mutation ; Peptide Library ; Protein Binding ; Protein Interaction Mapping/methods ; Transformation, Genetic ; Two-Hybrid System Techniques ; Workflow
Chemical Substances	KRIT1 Protein ; KRIT1 protein, human ; Peptide Library
Language	English
Publishing date	2020-06-10
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-0640-7_20
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Article: Patterns of Ciliation and Ciliary Signaling in Cancer.

Kiseleva, Anna A / Nikonova, Anna S / Golemis, Erica A

Reviews of physiology, biochemistry and pharmacology

2020 Volume 185, Page(s) 87–105

Abstract: Among the factors that have been strongly implicated in regulating cancerous transformation, the primary monocilium (cilium) has gained increasing attention. The cilium is a small organelle extending from the plasma membrane, which provides a localized ... ...

Abstract	Among the factors that have been strongly implicated in regulating cancerous transformation, the primary monocilium (cilium) has gained increasing attention. The cilium is a small organelle extending from the plasma membrane, which provides a localized hub for concentration of transmembrane receptors. These receptors transmit signals from soluble factors (including Sonic hedgehog (SHH), platelet-derived growth factor (PDGF-AA), WNT, TGFβ, NOTCH, and others) that regulate cell growth, as well as mechanosensory cues provided by flow or extracellular matrix. Ciliation is regulated by cell cycle, with most cells that are in G0 (quiescent) or early G1 ciliation and cilia typically absent in G2/M cells. Notably, while most cells organized in solid tissues are ciliated, cancerous transformation induces significant changes in ciliation. Most cancer cells lose cilia; medulloblastomas and basal cell carcinomas, dependent on an active SHH pathway, rely on ciliary maintenance. Changes in cancer cell ciliation are driven by core oncogenic pathways (EGFR, KRAS, AURKA, PI3K), and importantly ciliation status regulates functionality of those pathways. Ciliation is both influenced by targeted cancer therapies and linked to therapeutic resistance; recent studies suggest ciliation may also influence cancer cell metabolism and stem cell identity. We review recent studies defining the relationship between cilia and cancer.
MeSH term(s)	Humans ; Hedgehog Proteins/metabolism ; Signal Transduction/physiology ; Cell Cycle/physiology ; Cell Proliferation ; Neoplasms/metabolism ; Cilia/metabolism
Chemical Substances	Hedgehog Proteins
Language	English
Publishing date	2020-08-05
Publishing country	Germany
Document type	Review ; Journal Article
ZDB-ID	125106-5
ISSN	1617-5786 ; 0303-4240
ISSN (online)	1617-5786
ISSN	0303-4240
DOI	10.1007/112_2020_36
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Article: NEDD9 sustains hexokinase expression to promote glycolysis.

Deneka, Alexander Y / Nikonova, Anna S / Lee, Hyung-Ok / Kruger, Warren D / Golemis, Erica A

Oncogenesis

2022 Volume 11, Issue 1, Page(s) 15

Abstract: Elevated rates of glycolysis in cancer cells support tumor growth, in a process that typically depends on oncogene-induced increases in the expression and/or activity of enzymes in the glycolytic pathway. The NEDD9 scaffolding protein is upregulated in ... ...

Abstract	Elevated rates of glycolysis in cancer cells support tumor growth, in a process that typically depends on oncogene-induced increases in the expression and/or activity of enzymes in the glycolytic pathway. The NEDD9 scaffolding protein is upregulated in many advanced tumors, with increased NEDD9 promoting the activity of SRC and other effectors that promote invasion and metastasis. We here define a new role for NEDD9 in support of glycolysis. NEDD9 knockdown significantly impaired glycolysis in multiple lung cancer cell lines This was accompanied by post-transcriptional downregulation of steady-state levels of hexokinases (HK1 and HK2), which catalyze early steps in the glycolytic cascade, key rate limiting enzyme phosphofructokinase (PFK1), and downstream glyceraldehyde phosphate dehydrogenase (GAPDH). In mice, protein levels of HK1, HK2, PFK1, and GAPDH were depressed in Kras
Language	English
Publishing date	2022-04-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	2674437-5
ISSN	2157-9024
ISSN	2157-9024
DOI	10.1038/s41389-022-00391-w
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Article: Musashi-2 (MSI2) regulation of DNA damage response in lung cancer.

Bychkov, Igor / Deneka, Alexander / Topchu, Iuliia / Pangeni, Rajendra P / Lengner, Christopher / Karanicolas, John / Golemis, Erica A / Makhov, Petr / Boumber, Yanis

bioRxiv : the preprint server for biology

2023

Abstract: Lung cancer is one of the most common types of cancers worldwide. Non-small cell lung cancer (NSCLC), typically caused by : Significance: This study shows the novel role of Musashi-2 as regulator of ATM expression and DDR in lung cancer. ...

Abstract	Lung cancer is one of the most common types of cancers worldwide. Non-small cell lung cancer (NSCLC), typically caused by Significance: This study shows the novel role of Musashi-2 as regulator of ATM expression and DDR in lung cancer.
Language	English
Publishing date	2023-06-14
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.06.13.544756
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