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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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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.

2023-08-07 | GSE240199 | GEO

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.

2017-03-20 | PXD005309 | Pride

Mouse BM ILC progenitor subsets

Project description:Mouse BM ILC progenitor subsets

| PRJNA798063 | ENA

Effects of SPOP on gene expression in prostate cancer

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.

2014-10-10 | E-GEOD-59432 | biostudies-arrayexpress

Rhizobium sp. RM strain:RM

Project description:Rhizobium sp. RM strain:RM Genome sequencing and assembly

| PRJNA641501 | ENA

Deinococcus sp. RM strain:RM

Project description:Deinococcus sp. RM strain:RM Genome sequencing and assembly

| PRJNA489992 | ENA

Stable over expression of the SPOP-substrate ZMYND11 in VCaP cells

Project description:SPOP is known to bind to serine/theronine-rich degrons on substrate proteins. We identified two degron sequences within the PWWP and MYND domain of ZMYND11, a novel SPOP substrate, and investigated whether ZMYND11 may contribute to the transcriptional output of mutant SPOP in VCaP cancer cells. Hence, we performed over-expression of degron-deficient ZMYND11 and degron-deficient ZMYND11 with W294A mutation in VCaP cells. While WT ZMYND11 constructs can be robustly over-expressed at the mRNA level, only the degron-deficient variants yielded a robost increase in ZMYND11 protein expression. Degron mutant-induced transcriptional perturbations partially mimicked SPOP mutant-induced gene expression changes, suggesting that ZMYND11 is sufficient to recapitulate certain features of mutant SPOP.

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.

2018-10-03 | GSE100743 | GEO

Identification of ZMYND11 binding sites in VCaP cells with stable overexpression of either mutant (Y87C) or wild-type SPOP.

Project description:SPOP is known to bind to serine/theronine-rich degrons on substrate proteins. We identified two degron sequences within the PWWP and MYND domain of ZMYND11, a novel SPOP substrate, and investigated whether ZMYND11 may contribute to the transcriptional output of mutant SPOP in VCaP cancer cells. We mapped the genomic occupancy of ZMYND11 in VCaP cells over-expressing either wild type SPOP or the recurrent SPOP-Y87C mutant by ChIPseq. Genomic binding sites in the SPOP-Y87C mutant were increased over wild type SPOP, consistent with the increased ZMYND11 expression levels in the former.

2020-12-05 | E-MTAB-7174 | biostudies-arrayexpress

Stable overexpression and knockdown of mutant- or wild type SPOP in VCaP prostate cancer cells

Project description:Purpose: Little is known about the interplay of driver mutations that never co-occur within the same cancer cells. The latter scenario has been identified in prostate cancer where recurrent gene fusions involving the oncogenic ERG transcription factor and point mutations in the ubiquitin ligase adaptor SPOP are strictly mutually exclusive. We show that ERG and mutant SPOP – even though oncogenic on their own – are together synthetic sick. Description: RNA-Seq of lentiviral-transduced VCaP cells with stable knockdown of wild type SPOP (2 x hairpins) or stable overexpression of either wild-type or mutant SPOP (Y87C, F102C, W131G).

2020-12-05 | E-MTAB-7165 | biostudies-arrayexpress

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