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Genes, Vol. 12, Pages 1373: High Frequency of Tumor Propagating Cells in Fusion-Positive Rhabdomyosarcoma
In this study we investigated the expression of key stem cell markers, developed a sphere assay, and investigated the seven most common FPRMS cell lines for subpopulations of tumor propagating cancer stem-like cells, also called cancer stem cells (CSCs). Moreover, loss- and gain-of-functions of the stem cell genes SOX2, OCT4, and NANOG were investigated in the same cells. Single-cell clonal analysis was performed in vitro as well as in vivo. We found that no stable CSC subpopulation could be enriched in FPRMS. Unlike depletion of PAX3-FOXO1, neither overexpression nor siRNA-mediated downregulation of SOX2, OCT4, and NANOG ...
Source: Genes - August 31, 2021 Category: Genetics & Stem Cells Authors: Melanie Generali Sampoorna Satheesha Peter K. Bode Debora Wanner Beat W. Sch äfer Elisa A. Casanova Tags: Article Source Type: research

Pharmacologic Inhibition of Ezrin-Radixin-Moesin Phosphorylation is a Novel Therapeutic Strategy in Rhabdomyosarcoma.
This study investigates the inhibition of ERM phosphorylation using a small molecule pharmacophore NSC668394 as a potential strategy against RMS. Upon in vitro treatment with NSC668394, RMS cells exhibit a dose-dependent decrease in cell viability and proliferation, with induction of caspase-3 cleavage and apoptosis. siRNA-mediated knockdown of individual ERM protein expression revealed that each regulates RMS survival to a different degree. In vivo administration of NSC668394 in RMS xenografts causes significant decrease in tumor growth, with no adverse effect on body weight. Collectively, this study highlights the import...
Source: Sarcoma - October 3, 2020 Category: Cancer & Oncology Tags: Sarcoma Source Type: research

GSE140040 Next-generation sequencing reveals a novel role of lysine-specific demethylase 1 in adhesion of rhabdomyosarcoma cells RNA-seq
This study aims at elucidating changes in the RNA expression profile by RNA Sequencing in control and LSD1 knockdown conditions using transient silencing with siRNA. In addition, ChIP Sequencing was employed to investigate changes in the histone methylation pattern of H3K4me2 as a target of LSD1 in control and LSD1 knockdown conditions.
Source: GEO: Gene Expression Omnibus - November 7, 2019 Category: Genetics & Stem Cells Tags: Expression profiling by high throughput sequencing Homo sapiens Source Type: research

GSE140039 Next-generation sequencing reveals a novel role of lysine-specific demethylase 1 in adhesion of rhabdomyosarcoma cells ChIP-seq
This study aims at elucidating changes in the RNA expression profile by RNA Sequencing in control and LSD1 knockdown conditions using transient silencing with siRNA. In addition, ChIP Sequencing was employed to investigate changes in the histone methylation pattern of H3K4me2 as a target of LSD1 in control and LSD1 knockdown conditions.
Source: GEO: Gene Expression Omnibus - November 7, 2019 Category: Genetics & Stem Cells Tags: Genome binding/occupancy profiling by high throughput sequencing Homo sapiens Source Type: research

Macropinocytosis Dependent Entry of Chikungunya Virus into Human Muscle Cells
This study shows for the first time, that the infectious entry of CHIKV into human muscle cells is mediated by macropinocytosis. Together, the da ta from this study may pave the way for the development of specific inhibitors that target the entry process of CHIKV into cells.
Source: PLoS Neglected Tropical Diseases - August 25, 2019 Category: Tropical Medicine Authors: Ching Hua, Regina Lee Source Type: research

Susceptibility of Enterovirus-D68 to RNAi-mediated antiviral knockdown
Publication date: Available online 20 July 2019Source: Antiviral ResearchAuthor(s): Nicholas Klaiber, Michael A. McVoy, Wei ZhaoAbstractEnterovirus D68 (EV-D68) represents an emerging pathogen which has demonstrated a capacity for causing epidemic illness in pediatric and immunocompromised patients. With no effective antiviral treatment available, therapeutic interventions are currently limited to supportive care. Utilizing available genomic sequences from the 2014 B3 Epidemic EV-D68 clade and the 1962 Fermon EV-D68 strains, we performed in silico comparative genomic analysis, identifying several islands of phylogenetic co...
Source: Antiviral Therapy - July 21, 2019 Category: Virology Source Type: research

Susceptibility of Enterovirus-D68 to RNAi-mediated antiviral knockdown.
Abstract Enterovirus D68 (EV-D68) represents an emerging pathogen which has demonstrated a capacity for causing epidemic illness in pediatric and immunocompromised patients. With no effective antiviral treatment available, therapeutic interventions are currently limited to supportive care. Utilizing available genomic sequences from the 2014 B3 Epidemic EV-D68 clade and the 1962 Fermon EV-D68 strains, we performed in silico comparative genomic analysis, identifying several islands of phylogenetic conservation within the viral RNA-dependent RNA polymerase gene. The effects of transfecting short-interfering double-st...
Source: Antiviral Research - July 19, 2019 Category: Virology Authors: Klaiber N, McVoy MA, Zhao W Tags: Antiviral Res Source Type: research

Complement C5b-9 and Cancer: Mechanisms of Cell Damage, Cancer Counteractions, and Approaches for Intervention
In conclusion, osmotic burst of inflated complement-damaged cells may occur, but these bursts are most likely a consequence of metabolic collapse of the cell rather than the cause of cell death. The Complement Cell Death Mediator: A Concerted Action of Toxic Moieties Membrane pores caused by complement were first visualized by electron microscopy on red blood cell membranes as large ring structures (22). Similar lesions were viewed on E. coli cell walls (23). Over the years, ample information on the fine ultrastructure of the MAC that can activate cell death has been gathered (24) and has been recently further examined (...
Source: Frontiers in Immunology - April 9, 2019 Category: Allergy & Immunology Source Type: research

Targeting ALK in pediatric RMS does not induce antitumor activity in vivo
ConclusionsWhile ALK appears to be a relevant target in RMS in vitro, targeting this kinase in vivo yields no therapeutic efficacy, warranting extreme caution when considering the use of these agents in pediatric RMS patients.
Source: Cancer Chemotherapy and Pharmacology - May 31, 2018 Category: Cancer & Oncology Source Type: research

Hedgehog signaling negatively co-regulates BH3-only protein Noxa and TAp73 in TP53-mutated cells
In the present study, we show that pharmacological repression by the Hedgehog (Hh) pathway inhibitor (HPI) GANT61 induces expression of the proapoptotic protein Noxa in TP53-mutated embryonal pediatric tumor cells driven by Hh signaling (i.e. rhabdomyosarcoma (RMS) and medulloblastoma (MB)). Similarly, genetic silencing of Gli1 by siRNA causes increased Noxa mRNA and protein levels, while overexpression of Gli1 results in decreased Noxa expression. Furthermore, TAp73 mRNA and protein levels are increased upon Gli1 knockdown, while Gli1 overexpression reduces TAp73 mRNA and protein levels.
Source: Cancer Letters - April 24, 2018 Category: Cancer & Oncology Authors: Michael Torsten Meister, Cathinka Boedicker, Thomas Klingebiel, Simone Fulda Tags: Original Articles Source Type: research

MET/ERK2 pathway regulates the motility of human alveolar rhabdomyosarcoma cells.
In this study, we demonstrated the functions of MET signaling in ARMS in vitro by using three human ARMS cell lines and three human embryonal rhabdomyosarcoma (ERMS) cell lines. MET mRNA levels and MET protein expression in ARMS cell lines was higher than those in ERMS cell lines as detected by real-time quantitative PCR and western blotting, respectively. Based on cell growth and cell cycle analyses it was found that HGF stimulation did not enhance the proliferation of ERMS or ARMS cell lines. HGF-stimulated cell motility of ARMS cell lines was inhibited by U0126 (ERK1/2 inhibitor) but was only partially inhibited by PD9...
Source: Oncology Reports - November 16, 2016 Category: Cancer & Oncology Tags: Oncol Rep Source Type: research

FOXM1 expression in rhabdomyosarcoma: a novel prognostic factor and therapeutic target
This study aimed to determine the role of FOXM1 in RMS. We investigated the expression levels of FOXM1 and vascular endothelial growth factor (VEGF) and angiogenesis in a large series of RMS clinical cases using immunohistochemistry (n = 92), and we performed clinicopathologic and prognostic analyses. In vitro studies were conducted to examine the effect of FOXM1 knock-down on VEGF expression, cell proliferation, migration, and invasion in embryonal RMS (ERMS) and alveolar RMS (ARMS) cell lines, using small interference RNA (siRNA). High FOXM1 expression was significantly increased in the cases of ARMS, which has an ad...
Source: Tumor Biology - November 9, 2015 Category: Cancer & Oncology Source Type: research

Targeting of PAX3-FOXO1 by PLK1 Inhibition
In this report, we addressed this challenge by developing a two-armed screen for druggable upstream regulatory kinases in the PAX3/7-FOXO1 pathway. Screening libraries of kinome siRNA and small molecules, we defined PLK1 as an upstream-acting regulator. Mechanistically, PLK1 interacted with and phosphorylated PAX3-FOXO1 at the novel site S503, leading to protein stabilization. Notably, PLK1 inhibition led to elevated ubiquitination and rapid proteasomal degradation of the PAX3-FOXO1 chimeric oncoprotein. On this basis, we embarked on a preclinical validation of PLK1 as a target in a xenograft mouse model of aRMS, where the...
Source: Cancer Research - January 4, 2015 Category: Cancer & Oncology Authors: Thalhammer, V., Lopez–Garcia, L. A., Herrero–Martin, D., Hecker, R., Laubscher, D., Gierisch, M. E., Wachtel, M., Bode, P., Nanni, P., Blank, B., Koscielniak, E., Schafer, B. W. Tags: Molecular and Cellular Pathobiology Source Type: research

Abstract 3966: PLK1 regulates PAX3-FOXO1 stability and its inhibition mediates regression of alveolar rhabdomyosarcoma xenograft tumors
Oncogenic addiction provides an opportunity to develop new treatment options, especially for childhood cancers. Pediatric tumors contain a lower number of oncogenic mutations compared to most adult cancers, suggesting stronger dependency on individual oncogenes, such as chimeric transcription factors that have the ability to control multiple oncogenic pathways. Taking advantage of this addiction, targeting of oncogenic transcription factors becomes a new powerful strategy for therapy of translocation positive pediatric tumors like alveolar rhabdomyosarcoma (aRMS), which is characterized by a very dismal prognosis. As trans...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Thalhammer, V., Herrero–Martin, D., Hecker, R., Laubscher, D., Lopez–Garcia, L., Wachtel, M., Bode, P., Schafer, B. Tags: Tumor Biology Source Type: research