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Comparison of RNA-seq and Microarray Platforms for Splice Event Detection using a Cross-Platform Algorithm [Junction Arrays]

ABSTRACT: In this study, we compare the performance of RNA-seq (Illumina HiSeq) and junction arrays (Affymetrix Human Transcriptome array) for the analysis of splicing events. Three different cell lines were treated with CX-4945, a drug that severely affects splicing. To make a fair comparison, we developed EventPointer, an algorithm that detects and labels alternative splicing events in both junction arrays and RNA-seq. Common results and discrepancies between both technologies were validated or resolved by more than 200 PCRs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE104610 | GEO | 2018/09/05

REPOSITORIES: GEO

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Comparison of RNA-seq and Microarray Platforms for Splice Event Detection using a Cross-Platform Algorithm [RNA-Seq]

Project description:In this study, we compare the performance of RNA-seq (Illumina HiSeq) and junction arrays (Affymetrix Human Transcriptome array) for the analysis of splicing events. Three different cell lines were treated with CX-4945, a drug that severely affects splicing. To make a fair comparison, we developed EventPointer, an algorithm that detects and labels alternative splicing events in both junction arrays and RNA-seq. Common results and discrepancies between both technologies were validated or resolved by more than 200 PCRs.

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Compound-induced NR5A1 exon-skipping and circular-RNA expression show impaired steroidogenesis in adrenocortical cancer cells

Project description:Despite the intensive search for an effective drug to treat steroid-producing adrenocortical carcinomas, there are few therapeutic options. We sought whether splicing modifying compounds are effective on this devastating disease. Here, we show that a chemical compound in clinical trial, CX-4945, suppressed the expression of NR5A1 through aberrant multiple exon skipping leading to suppressed steroidogenesis and induced dysfunctional autophagy and progression to ER-stress-related apoptosis. A circular RNA of NR5A1 exons with an IRE1α-cleavage site on the ligated ends (circAd4BP HAC1-type ex1-6 RNA) is expressed in normal adrenal cortex but not in H295R adrenocortical cancer cells, and CX-4945 induced a different circular RNA of NR5A1 exons (circAd4BP ex2-4 RNA). This potential pharmacological control of abnormal steroidogenesis through NR5A1 aberrant splicing and interplay with its circAd4BP makes CX-4945 a strong candidate novel drug for the treatment of adrenocortical carcinomas.

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Whole methylome analysis of SEM cell lines

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Protein Kinase CK2 Controls the Fate Between Th17 Cell and Regulatory T Cell Differentiation

Project description:We report that CK2 inhibition with CX-4945 broadly suppresses Th17-associated effector and metabolic gene expression. CD4+ T cells were cultured in IL-6, IL-23 and TGFb1 for 72 h, in the absence of presence of 2 mM CX-4945, RNA-seq was performed and gene expression compared between the control and treatment groups.

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Cooperative blockade of CK2 and ATM kinases drives apoptosis in VHL-deficient renal carcinoma cells / RNA-seq (BRB-seq) of treated 786-O spheroids

Project description:Multicellular Tumor Spheroids (MCTS) were pre-formed for 3 days with 786-O cell line to better mimic the tumor microenviroenment. These spheroids were treated with either vehicle (DMSO), drugs alone (KU-60019 10 μM; CX-4945 5 μM) or in combination (KU + CX) for 48h before RNA extraction.

2021-02-04 | E-MTAB-9977 | biostudies-arrayexpress

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Project description:EventPointer: An effective identification of alternative splicing events using junction arrays

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Identification of miRNAs that mediate protective function of anti-cancer drugs during white matter ischemic injury

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Comparison of CX-4945 and SCG-CK2-1 as Inhibitors of CSNK2 using Quantitative Phosphoproteomics: Triple SILAC in combination with Inhibitor-Resistant CSNK2

Project description:Specificity is a limiting factor when using small-molecule inhibitors to study protein kinase signalling. Since inhibitor-resistant kinase mutants (i.e., drug-resistant alleles) remain active in the presence of inhibitor, they facilitate validation of on-target effects. By combining an inhibitor-resistant kinase mutant with mass spectrometry-based phosphoproteomics, we previously devised a systematic strategy for reliable identification and validation of CSNK2 substrates. In this study, we use the same strategy to evaluate the selectivity of CX-4945, a clinical stage CSNK2 inhibitor, and SGC-CK2-1, a chemical probe selectively targeting CSNK2. Human osteosarcoma (U2OS) cells expressing exogenous wild-type CSNK2A1 (WT) or an inhibitor-resistant triple mutant (TM, V66A/H160D/I174A) were treated with CX-4945 or SGC-CK2-1 prior to analysis using triple SILAC (phospho)proteomics. The minority of phosphosites, 15% at 4 hours and 5% at 24 hours, that were significantly downregulated in response to CX-4945 treatment were determined to be CSNK2A1-dependent. By comparison, the majority of phosphosites, >55% at both 4 and 24 hours, that were significantly downregulated in response to SGC-CK2-1 were identified as CSNK2A1-dependent. This indicates that SGC-CK2-1 exhibits dramatically greater selectivity towards CSNK2A1 than CX-4945. Notably, utilization of SGC-CK2-1 in cells expressing TM-CSNK2A1 enabled the identification of 330 CSNK2A1-dependent phosphosites. Overall, this study highlights the utility of exploiting highly selective chemical probes together with inhibitor-resistant kinase mutants to identify bona fide kinase substrates.

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Comparison of RNA-seq and Microarray Platforms for Splice Event Detection using a Cross-Platform Algorithm [Junction Arrays]

Project description:Comparison of RNA-seq and Microarray Platforms for Splice Event Detection using a Cross-Platform Algorithm [Junction Arrays]

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Ikaros and CK2 regulate expression of Bcl-xL and chemosensitivity in high-risk B-cell acute lymphoblastic leukemia

Project description:High-risk B-cell acute lymphoblastic leukemia (B-ALL) is an aggressive disease, often characterized by resistance to chemotherapy. A frequent feature of high-risk B-ALL is loss of function of the Ikaros tumor suppressor. In leukemia, Ikaros’ function is impaired by oncogenic Casein Kinase II (CK2), which is overexpressed in B-ALL. Phosphorylation by CK2 reduces Ikaros binding to the promoter of its target gene, particularly Bcl-xL. This results in a loss of Ikaros-mediated repression of Bcl-xL and in increased expression of Bcl-xL. Increased expression of Bcl-xL and/or CK2, as well as reduced Ikaros expression, are associated with resistance to doxorubicin treatment. Molecular and pharmacological inhibition of CK2 with a specific inhibitor CX-4945, enhances Ikaros-mediated repression of Bcl-xL and increases sensitivity to doxorubicin. Combination treatment with CX-4945 and doxorubicin show synergistic therapeutic effects in vitro and in preclinical models of high-risk B-ALL. Results reveal a novel signaling network that regulates chemoresistance in leukemia and lays the groundwork for clinical testing of CK2 inhibitors in combination with doxorubicin for the treatment of hematopoietic malignancies.

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