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Murine hamatopoietic stem cell (HSC): wild type and Skp2 knockout

ABSTRACT: Transcriptional profiling of mouse HSC comparing wild type (WT) and Skp2 knockout Collected bone marrow (BM) cells from WT and Skp2 knockout mice, stained with HSC surface markers for FACS. Collected HSC and extracted total RNA then sent out for microarray analysis.

ORGANISM(S): Mus musculus

SUBMITTER: JING WANG

PROVIDER: E-GEOD-23064 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Skp2-macroH2A1-CDK8 axis orchestrates G2/M transition and tumorigenesis.

Xu Dazhi D Li Chien-Feng CF Zhang Xian X Gong Zhaohui Z Chan Chia-Hsin CH Lee Szu-Wei SW Jin Guoxiang G Rezaeian Abdol-Hossein AH Han Fei F Wang Jing J Yang Wei-Lei WL Feng Zi-Zhen ZZ Chen Wei W Wu Ching-Yuan CY Wang Ying-Jan YJ Chow Lu-Ping LP Zhu Xiao-Feng XF Zeng Yi-Xin YX Lin Hui-Kuan HK

Nature communications 20150330

Understanding the mechanism by which cell growth, migration, polyploidy, and tumorigenesis are regulated may provide important therapeutic strategies for cancer therapy. Here we identify the Skp2-macroH2A1 (mH2A1)-cyclin-dependent kinase 8 (CDK8) axis as a critical pathway for these processes, and deregulation of this pathway is associated with human breast cancer progression and patient survival outcome. We showed that mH2A1 is a new substrate of Skp2 SCF complex whose degradation by Skp2 promo ...[more]

PMID: 25818643

Publication: 1/2

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Murine hamatopoietic stem cell (HSC): wild type and Skp2 knockout

Project description:Transcriptional profiling of mouse HSC comparing wild type (WT) and Skp2 knockout

2015-04-02 | GSE23064 | GEO

SKP2 knockout in Rb1/p53 deficient transgenic mouse models of osteosarcoma induces macrophage infiltration and drives transcription of genes with favorable prognosis in patients

Project description:To study SKP2 in osteosarcoma, we generated a Skp2 KO line and a Skp2 intact line of transgenic OS mouse models: germline Skp2 knockout (“TKO”: Osx1-Cre;Rb1lox/lox;p53lox/lox;SKP2) versus Skp2 intact (“DKO”: Osx1-Cre;Rb1lox/lox;p53lox/lox). We then performed bulk RNAseq of the SKP2 KO vs SKP2 intact OS.

2023-10-02 | GSE226634 | GEO

MDAMB231 transcriptome response to SKP2 knockdown

Project description:The SKP2 was knockdown by siRNAs in MDA-MB231 cells and RNA-Seq was used to define the transcriptome response to SKP2

2020-12-14 | GSE163110 | GEO

Comprehensive single cell transcriptomics analysis of murine osteosarcoma uncovers Skp2 function in metastasis, genomic instability and immune activation and reveals additional target pathways

Project description:Osteosarcoma (OS) is the most common primary pediatric bone malignancy. One promising new therapeutic target is SKP2, encoding a substrate recognition factor of the SCF E3 ubiquitin ligase responsible for ubiquitination and proteasome degradation of substrate p27, thus driving cellular proliferation. We have shown previously that knockout of Skp2 in an immunocompetent transgenic mouse model of OS improved survival, drove apoptosis, and induced tumor inflammation. Here, we applied single-cell RNA-sequencing (scRNA-seq) to study primary OS tumors derived from Osx-Cre driven conditional knockout of Rb1 and Trp53. We showed that murine OS models recapitulate the tumor heterogeneity and microenvironment complexity observed in patient tumors. We further compared this model with OS models with functional disruption of Skp2: one with Skp2 knockout and the other with the Skp2-p27 interaction disrupted (resulting in p27 overexpression). We found reduction of T cell exhaustion and upregulation of interferon activation, along with evidence of replicative and endoplasmic reticulum-related stress in the Skp2 disruption models, and showed that interferon induction was correlated with improved survival in OS patients. Additionally, our scRNA-seq analysis uncovered decreased activities of metastasis-related gene signatures in the Skp2-modulated OS, which we validated by observation of a strong reduction in lung metastasis in the Skp2 knockout mice. Finally, we report several potential mechanisms of escape from targeting Skp2 in OS, including upregulation of Myc targets, DNA copy number amplification and overexpression of alternative E3 ligase genes, and potential alternative lineage activation. These mechanistic insights into OS tumor biology and Skp2 function suggest novel targets for new, synergistic therapies, while the data and our comprehensive analysis may serve as a public resource for further big data-driven OS research.

2024-06-28 | GSE262743 | GEO

SKP2-affinity-purified mass spectrometry analysis.

Project description:This project aims to identify the SKP2 interaction proteins.

2023-01-05 | PXD039225 | Pride

comparison_col0vsskp2-Functional analysis of the SKP2 and CUL4 proteins

Project description:rs04-04_skp2_cul4 - comparison_col0vsskp2 - Antisense and mutants of the SKP2 and CUL4 genes are compared to the Wt in order to identify the genes controlled by those SCF proteins. - Comparison Col0 versus skp2

2012-03-27 | GSE36651 | GEO

comparison_col0vsskp2-Functional analysis of the SKP2 and CUL4 proteins

2012-03-26 | E-GEOD-36651 | biostudies-arrayexpress

Mus musculus

Project description:Murine hamatopoietic stem cell (HSC): wild type and Skp2 knockout

| PRJNA129889 | ENA

MDAMB231 transcriptome response to SKP2 knockdown

Project description:MDAMB231 transcriptome response to SKP2 knockdown

| PRJNA684918 | ENA

A MYOD-SKP2 axis boosts tumorigenesis in fusion negative rhabdomyosarcoma by preventing differentiation through p57Kip2 targeting [Hi-ChIP]

Project description:Rhabdomyosarcoma (RMS) is a pediatric mesenchymal-derived malignancy encompassing Fusion Positive (FP)-RMS expressing PAX3/7-FOXO1 and Fusion Negative (FN)-RMS often mutated in the RAS pathway. RMS expresses the master myogenic transcription factor MYOD that, paradoxically, is unable to support differentiation while essential for tumor cell survival. We identify here SKP2, an oncogenic E3-ubiquitin ligase, as a critical driver of tumorigenesis in FN-RMS. SKP2 is overexpressed in RMS at the highest levels among several adult and pediatric cancers and its expression is maintained by MYOD through an intronic enhancer within the gene. In FN-RMS SKP2 promotes cell cycle progression and prevents differentiation directly targeting p27Kip1 and p57Kip2, respectively, unlocking a transcriptional myogenic program, partly MYOD-dependent, resulting in de novo expression of terminal muscle differentiation markers. SKP2 depletion strongly affects stemness and tumorigenic features in vitro and prevents in vivo tumor growth. The in vitro effects are mirrored by the SKP2 inhibitor SMIP004. Moreover, the investigational NEDDylation inhibitor MLN4924 hampers SKP2 functions restraining FN-RMS cell survival and tumor growth. Our results uncover a MYOD-SKP2 axis crucial for the crosstalk between transcriptional and post-translational mechanisms that contribute to FN-RMS tumorigenesis and broaden the understanding of MYOD function. Furthermore, they suggest inhibition of NEDDylation as a potential therapeutic approach in this tumor.

2023-10-16 | GSE245495 | GEO

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