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RIPK3 is a tumor suppressor in mesothelioma

ABSTRACT: RIPK3 is a tumor suppressor in mesothelioma

PROVIDER: PRJNA666445 | ENA |

REPOSITORIES: ENA

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RIPK3 is a tumor suppressor in mesothelioma

Project description:RIPK3 locus is methylated in mesothelioma cell lines

2021-02-24 | GSE158768 | GEO

RIPK3 Activation Induces TRIM28 Derepression in Cancer Cells and Enhances the Anti-tumor Microenvironment

Project description:We identified TRIM28 as a co-repressor that regulates transcriptional activity during necroptosis. RIPK3 activation induces TRIM28 phosphorylation at serine 473, inhibiting its chromatin binding activity, thereby contributing to the transactivation of NF-κB and other transcription factors, such as SOX9. This leads to elevated cytokine expression, which then potentiates immunoregulatory processes, such as DC maturation. The expression of RIPK3 has a significant positive association with the tumor-infiltrating immune cells populations in various tumor type, thereby activating anti-cancer responses.

2021-06-25 | GSE178847 | GEO

LCK-mediated RIPK3 Activation Controls Double-Positive Thymocyte Proliferation and Restrains Thymic Lymphoma by Regulating the PP2A-ERK Axis

Project description:Receptor-interacting protein kinase 3 (RIPK3) is the primary regulator of necroptotic cell death. RIPK3 expression is often silenced in various cancer cells, which suggests that it may have tumor suppressor properties. However, the exact mechanism by which RIPK3 negatively regulates cancer development and progression remains unclear. This report indicates that RIPK3 acts as a potent regulator of homeostatic proliferation of CD4+CD8+ double-positive (DP) thymocytes. Abnormal proliferation of RIPK3-deficient DP thymocytes occurs independently of the well-known role for RIPK3 in necroptosis (upstream of MLKL activation), and is associated with an incidental thymic mass, likely thymic hyperplasia. In addition, Ripk3-null mice developed increased thymic tumor formation accompanied by reduced host survival in the context of a N-ethyl-N-nitrosourea (ENU)-induced tumor model. Moreover, RIPK3 deficiency in p53-null mice promoted thymic lymphoma development via upregulated ERK signaling, which correlated with markedly reduced survival rates. Mechanistically, lymphocyte-specific protein tyrosine kinase (LCK) activates RIPK3, which in turn leads to increases in the phosphatase activity of protein phosphatase 2 (PP2A), thereby suppressing hyper-activation of ERK in DP thymocytes. Overall, these findings suggest that a RIPK3-PP2A-ERK signaling axis regulates DP thymocyte homeostasis and may provide a potential therapeutic target to improve thymic lymphoma therapies.

2022-09-18 | GSE213606 | GEO

Transcriptional profile of recurrent breast cancer cells with RIPK3 silencing

Project description:To understand to role of RIPK3 during tumor recurrence, we performed RNAseq to study the transcriptional response of mouse recurrent breast cancer cells to RIPK3 knockdown.

2020-01-27 | GSE124634 | GEO

Copy number variation analysis of desmoplastic malignant mesothelioma

Project description:Desmoplastic malignant mesothelioma is a rare tumor. Due to the rarity, genomic profile of desmoplastic malignant mesothelioma is not unveiled. To elucidate genomic profile of desmoplastic malignant mesothelioma, we used illumina infinium omini exomeexpress in an established patient-derived cell line of desmoplastic malignant mesothelioma.

2021-10-18 | GSE185549 | GEO

Mesothelioma-associated fibroblasts enhance proliferation and migration of malignant pleural mesothelioma cells via Met/PI3K and WNT signaling but do not protect against cisplatin

Project description:Malignant pleural mesothelioma (MPM) is an aggressive malignancy with poor prognosis. Unlike many other cancers, MPM is mostly characterized by inactivation of tumor suppressor genes. Its highly malignant nature in absence of tumor driving oncogene mutations indicates an extrinsic supply of stimulating signals by cells of the tumor microenvironment (TME). Cancer-associated fibroblasts (CAFs) are an abundant cell type of the TME and have been shown to drive the progression of several cancer types. The aim of the current study was to isolate and characterize patient-derived mesothelioma-associated fibroblasts (Meso-CAFs), and evaluate their impact on MPM cells.

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Gene Expression Profiling of Malignant Peritoneal Mesothelioma Patient Tumor Samples

2010-09-27 | GSE15627 | GEO

Gene Expression Profiling of Malignant Peritoneal Mesothelioma Patient Tumor Samples

Project description:Gene expression profiles were generated from 41 consecutive surgically resected fresh frozen malignant peritoneal mesothelioma patient tumor samples to identify molecular prognostic factors. Patient tumor samples hybridized against the common reference (complementary DNA generated from human universal RNA), 41 tumor samples.

2010-09-27 | E-GEOD-15627 | biostudies-arrayexpress

Gene Expression of Malignant Pleural Mesothelioma Tumor and paired Normal Lung tissue

Project description:In order to discover critical pathways /networks or therapeutic targets in pleural mesothelioma we profiled 55 tumors along with paired normal tissue (for 41 tumors) using Affymetrix U133 plus 2.0 chips RNA isolated from frozen resected tumor and normal tissues was hybridized to Affymetrix U133 plus 2.0 chips to discover genes upregulated/downregulated in mesothelioma tumors compared to paired normal non-tumor adjacent tissue as well as find differences between the different tumors

2014-08-31 | E-GEOD-51024 | biostudies-arrayexpress

Transcriptional profiles of PA1 teratoma cells transfected by RIPK1, RIPK2, RIPK3, or RIPK4

Project description:RIPK4 but not the related kinases RIPK1, RIPK2, and RIPK3 caused similar transcriptional changes to Wnt3a. PA1 cells were transfected by 8ug RIPK1, RIPK2, RIPK3, or RIPK4 for 48h, RNA were extracted and sequenced.

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