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Next Generation Sequencing analysis using SPOP mutant (F133V)-transduced RM-1-BM mouse prostate cancer cells and RAW264.7 mouse macrophage cells

ABSTRACT: Next Generation Sequencing analysis using SPOP mutant (F133V)-transduced RM-1-BM mouse prostate cancer cells and RAW264.7 mouse macrophage cells

PROVIDER: PRJNA1002794 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25541800_1.fastq.gz	Fastqsanger.gz
	SRR25541800_2.fastq.gz	Fastqsanger.gz
	SRR25541801_1.fastq.gz	Fastqsanger.gz
	SRR25541801_2.fastq.gz	Fastqsanger.gz
	SRR25541802_1.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing analysis using SPOP mutant (F133V)-transduced RM-1-BM mouse prostate cancer cells and RAW264.7 mouse macrophage cells

Project description:In this experiment, we analyzed the gene expression profiles of SPOP mutant (F133V)-transduced (and vector control) RM-1-BM mouse prostate cancer cells and RAW264.7 macrophage cells in transwell coculture and monoculture in the context of olaparib (or vehicle) treatment by RNA sequencing.

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SPOP mutation - SPOP Mutation Drives Prostate Tumorigenesis In Vivo through Coordinate Regulation of PI3K/mTOR and AR Signaling

Project description:Recurrent point mutations in SPOP define a distinct molecular subclass of prostate cancer. Here, we describe the first mouse model showing that mutant SPOP drives prostate tumorigenesis in vivo. Conditional expression of mutant SPOP in the prostate dramatically altered phenotypes in the setting of Pten loss, with early neoplastic lesions (high-grade prostatic intraepithelial neoplasia) with striking nuclear atypia, and invasive poorly differentiated carcinoma. In mouse prostate organoids, mutant SPOP drove increased proliferation and a transcriptional signature consistent with human prostate cancer. Using these models and human prostate cancer samples, we show that SPOP mutation activates both PI3K/mTOR and androgen receptor (AR) signaling, effectively uncoupling the normal negative feedback between these two pathways. Associated RNA-seq data deposited in GEO: GSE94839.

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Project description:SPOP is a ubiquitin ligase adaptor frequently mutated in prostate cancer. It is involved in ubiquitination and degradation of substrate proteins. We examined the impact of wild-type and mutant SPOP on the transcriptional profile of prostate cancer cells. We cloned several naturally occurring (in human prostate cancer) SPOP mutants and expressed the corresponding constructs in prostate cancer cells. Our experimental conditions were: Human prostate cancer cells (LNCaP-Abl), transfected with control vector, SPOP-wt, and any of the following mutants: SPOP-F102C, SPOP-F133V, SPOP-F133L (2-4 biological replicates each). We analyzed their gene expression profiles for differences induced by SPOP-wt vs SPOP-mutant.

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E3 ligase substrate adaptor SPOP fine tunes the UPR of pancreatic beta cells

Project description:The Cullin 3 E3 ligase adaptor protein, SPOP, targets proteins for ubiquitination and proteasomal degradation. We previously established the β cell transcription factor (TF) and human diabetes gene PDX1 as an SPOP substrate, suggesting a functional role for SPOP in the β cell. Here, we generated a β cell specific Spop deletion mouse strain (SpopβKO) and found that Spop is necessary to prevent aberrant basal insulin secretion and for maintaining glucose- stimulated insulin secretion (GSIS) through impacts on glycolysis and glucose-stimulated calcium flux. Integration of proteomic, TF-regulatory gene network and biochemical analyses identified XBP1 as a functionally important SPOP substrate in pancreatic β cells.Further, loss of SPOP strengthened the IRE1α-XBP1 axis of unfolded protein response (UPR) signaling. ER stress promoted proteasomal degradation of SPOP, supporting a model whereby SPOP fine-tunes XBP1 activation during the UPR. These results position SPOP as a regulatorof β cell function and proper UPR activation.

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E3 ligase substrate adaptor SPOP fine tunes the UPR of pancreatic beta cells

Project description:The Cullin-3 E3 ligase adaptor protein, SPOP, targets proteins for ubiquitination and proteasomal degradation. We previously established the β cell transcription factor (TF) and human diabetes gene PDX1 as an SPOP substrate, suggesting a functional role for SPOP in the β cell. Here, we generated a β cell specific Spop deletion mouse strain (SpopβKO) and found that Spop is necessary to prevent aberrant basal insulin secretion and for maintaining glucose- stimulated insulin secretion (GSIS) through impacts on glycolysis and glucose-stimulated calcium flux. Integration of proteomic, TF-regulatory gene network and biochemical analyses identified XBP1 as a functionally important SPOP substrate in pancreatic β cells. Further, loss of SPOP strengthened the IRE1α-XBP1 axis of unfolded protein response (UPR) signaling. ER stress promoted proteasomal degradation of SPOP, supporting a model whereby SPOP fine-tunes XBP1 activation during the UPR. These results position SPOP as a regulator of β cell function and proper UPR activation.

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2020-12-16 | E-MTAB-7173 | biostudies-arrayexpress

Gene Expression Profiling of SPOP Knocked Down Cell

Project description:SPOP is one of the most frequent mutated genes in prostate cancer. In the current study, we identified CCNE1 as its substrate. SPOP directly interacts with CCNE1, poly-ubiquitinates CCNE1 in vivo and in vitro, and represses cancer-related phenotypes induced by CCNE1 expression. Thus, we reveal a new mechanism for SPOP in repressing prostate cancer tumorigenesis.

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