Estrogen-related receptor beta activation and isoform shifting by cdc2-like kinase inhibition restricts migration and intracranial tumor growth in glioblastoma

Tiek, DM; Khatib, SA; Trepicchio, CJ; Heckler, MM; Divekar, SD; Sarkaria, JN; Glasgow, Eric; Riggins, Rebecca B.

doi:10.1101/558775

Cited by 2 publications

(1 citation statement)

References 54 publications

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“…Zebrafish xenografts assays have been frequently incorporated into studies on the control of cancer growth, invasion, and migration. Components of cancer-related pathways have been altered by gene mutations [34,35], gene overexpression or knockdown [35][36][37][38][39][40][41][42], protein inactivation by antibody binding [41], pharmacological inhibition of protein function [34,36,42,43], and cell culture selection for drug resistance [32,43]. In many of these studies, zebrafish xenograft models were run in parallel with mouse models, which reported comparable results [34,[36][37][38][41][42][43].…”

Section: Zebrafish Xenografts Clarify the Mechanistic Underpinnings Of Tumor Cell Behaviors And Their Interactions With The Cancer-associmentioning

confidence: 99%

Zebrafish Xenografts for Drug Discovery and Personalized Medicine

2020

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Cancer is the second leading cause of death in the world. Given that cancer is a highly individualized disease, predicting the best chemotherapeutic treatment for individual patients can be difficult. Ex vivo models such as mouse patientderived xenografts (PDX) and organoids are being developed to predict patient-specific chemosensitivity profiles before treatment in the clinic. Although promising, these models have significant disadvantages including long growth times that introduce genetic and epigenetic changes to the tumor. The zebrafish xenograft assay is ideal for personalized medicine. Imaging of the small, transparent fry is unparalleled among vertebrate organisms. In addition, the speed (5-7 days) and small patient tissue requirements (100-200 cells per animal) are unique features of the zebrafish xenograft model that enable patient-specific chemosensitivity analyses. Zebrafish Have Become a Leading Animal Model for Human Disease and Personalized MedicineFifty years ago, George Streisinger took a leap of faith. He chose a fish for his vertebrate genetic model organism (see Glossary). Many of his contemporaries believed that a fish would be too evolutionarily distant from mammals to have any relevance for human health, and that he would only learn about the genetics of fish [1]. We have since learned that zebrafish and humans have more in common than not. For example, zebrafish retain most of the same organs ('two eyes, mouth, brain, spinal cord, intestine, pancreas, liver, bile ducts, kidney, esophagus, heart, ear, nose, muscle, blood, bone, cartilage, and teeth') but notably lack lungs. Zebrafish would therefore be unsuitable for the development of lung disease models (although they would make an excellent lung cancer metastasis model) [2]. Publication of the complete zebrafish genome in 2013 showed that 70% of the genes in zebrafish have human orthologs, and cross-comparison of disease-related genes annotated in the Online Mendelian Inheritance in Man (OMIM) database reveals that 82% of those genes have at least one zebrafish ortholog [2,3]. HighlightsZebrafish xenografts are proven models of human cancer biology that provide rapid in vivo validation of anticancer drugs and drug targets.Zebrafish have emerged as unsurpassed models for imaging tumor metastasis.

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Section: Zebrafish Xenografts Clarify the Mechanistic Underpinnings Of Tumor Cell Behaviors And Their Interactions With The Cancer-associmentioning

confidence: 99%

Zebrafish Xenografts for Drug Discovery and Personalized Medicine

2020

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Splicing Dysregulation as Oncogenic Driver and Passenger Factor in Brain Tumors

Bielli

Pagliarini

Pieraccioli

et al. 2019

Cells

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Brain tumors are a heterogeneous group of neoplasms ranging from almost benign to highly aggressive phenotypes. The malignancy of these tumors mostly relies on gene expression reprogramming, which is frequently accompanied by the aberrant regulation of RNA processing mechanisms. In brain tumors, defects in alternative splicing result either from the dysregulation of expression and activity of splicing factors, or from mutations in the genes encoding splicing machinery components. Aberrant splicing regulation can generate dysfunctional proteins that lead to modification of fundamental physiological cellular processes, thus contributing to the development or progression of brain tumors. Herein, we summarize the current knowledge on splicing abnormalities in brain tumors and how these alterations contribute to the disease by sustaining proliferative signaling, escaping growth suppressors, or establishing a tumor microenvironment that fosters angiogenesis and intercellular communications. Lastly, we review recent efforts aimed at developing novel splicing-targeted cancer therapies, which employ oligonucleotide-based approaches or chemical modulators of alternative splicing that elicit an impact on brain tumor biology.

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Estrogen-related receptor beta activation and isoform shifting by cdc2-like kinase inhibition restricts migration and intracranial tumor growth in glioblastoma

Cited by 2 publications

References 54 publications

Zebrafish Xenografts for Drug Discovery and Personalized Medicine

Zebrafish Xenografts for Drug Discovery and Personalized Medicine

Splicing Dysregulation as Oncogenic Driver and Passenger Factor in Brain Tumors

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