Identification of RNF4 dependent gene signature in melanoma tumors
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA510643 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8350410.fastq.gz | Fastqsanger.gz | |||
| SRR8350420.fastq.gz | Fastqsanger.gz | |||
| SRR8350430.fastq.gz | Fastqsanger.gz | |||
| SRR8350440.fastq.gz | Fastqsanger.gz | |||
| SRR8350411.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 36 |
Similar Datasets
Project description:Among hallmarks of cancer is impaired proteostasis, that is characterized by increased oncoprotein stability. Here we demonstrate that RNF4, a ubiquitin ligase implicated in the stabilization of short-lived oncoproteins, is important for melanoma tumorigenesis. High levels of RNF4 in melanoma patient-derived specimens coincide with poor prognosis. Accordingly, RNF4, is essential for the growth and migration and survival of melanoma cells, both in culture and in xenograft models. RNA-seq analyses of RNF4-expressing tumors identified a gene signature related to melanoma growth and migration. Among the upstream regulators of RNF4-dependent gene signature are c-Myc and HIF1a which exhibit elevated protein levels that also coincided with stabilization of the translation initiation regulator p-eIF2a. Correspondingly, the effects of RNF4 on melanomagenesis are p-eIF2a-dependent, thus highlighting an unexpected regulatory axis in melanoma via RNF4-and ubiquitin-dependent protein stabilization
2021-05-05 | GSE124064 | GEO
Project description:Molecular understanding of osteogenic differentiation (OD) of human bone-marrow derived mesenchymal stem cells (hBMSCs) is important for regenerative medicine and has direct implications to cancer. Here we report that the RNF4 ubiquitin ligase is essential for OD of hBMSCs, and that RNF4 deficient hBMSCs fail to differentiate and remain as stalled progenitors. Remarkably, addition of media from differentiating hBMSCs to RNF4-deficient MSCs alleviated the block in OD. Transcriptional analysis of RNF4-dependent gene signature identified two secreted factors; BMP6 and the guidance molecule BMP6 co-receptor RGMb (Dragon). Knockdown of either RGMb or BMP6 in hBMSCs inhibit differentiation, and only the combined addition of purified RGMb and BMP6 proteins to RNF4-deficient MSCs fully restored osteogenic differentiation. Moreover, RNF4-RGMb axis is highly relevant cancer cell survival and tumorigenicity, including osteosarcoma and Therapy-resistant melanoma cells. In accordance, in human melanoma biopsies high level of RGMb correlates with high level of RNF4, and is associated with resistance to molecular therapy and poor prognosis of patients. Thus, RNF4~BMP6~RGMb is a molecular axis that is key for OD and tumorigenesis.
2022-09-28 | GSE205432 | GEO
Project description:Melanoma is the most aggressive form of skin cancer with estimated 48,000 deaths worldwide. The polyphenol curcumin derived from the plant Curcuma longa is well known for its anti-inflammatory and anti-cancerogenic properties. Accordingly, dietary intake of this compound may be suitable for melanoma prevention. However, how this compound affects basic cellular mechanisms in developing melanoma still remains elusive. Therefore, the aim of this study was to investigate for the first time the impact of oral curcumin administration on the miRNA signature of engrafting melanoma. For this purpose, the effects of a 4% curcumin diet on murine B78H1 melanoma were tested in a flank model. Curcumin diet or standard chow (control) was administered two weeks prior to tumor initiation until termination of the experiment. Highly significant chip-based miRNA array analysis was deployed to detect alterations in the miRNA signature of the tumors. Curcumin treatment significantly reduced the growth of the flank tumors. Furthermore the miRNA expression signature in tumors was substantially altered by curcumin intake with mmu-miR-205-5p over 100 times higher expressed when compared to controls. Putative targets of curcumin-induced up-regulated miRNAs were enriched in o-glycan biosynthesis, endoplasmatic reticulum protein processing and different cancer-related pathways. These findings demonstrate a profound alteration of the miRNA expression signature in engrafting curcumin-treated melanoma with mmu-miR-205-5p being up-regulated most significantly. Treatment of male C57BL/6 mice with induced flank tumors (injection of B78H1 cells) either with standard mouse chow (control n=6) or chow enriched with 4% of curcumin (treatment group n=7 )
2013-12-31 | E-GEOD-47211 | biostudies-arrayexpress
Project description:GSK3685032-induced DNA hypomethylation results in upregulation of largely viral-responsive gene expression pathways and cell death. We identified that loss of RNF4 causes resistance to GSK3685032. We established RNF4 wild type and deficient MV4-11 cells by CRISPR-Cas9 disruption and treated with vehicle or GSK3685032 to determine how RNF4-deficiency impacts GSK3685032-induced gene expression changes
2026-05-17 | GSE233727 | GEO
Project description:In this project we aim to identify the spacific targets of the SUMO-Targeted Ubiquitin Ligase (STUBL) RNF4. For that, we combine the study of SUMOylation targets that are enriched after RNF4 knockdown with the use of Targeted Ubiquitin Ligases Identified by Proteomics (TULIP).
2017-11-23 | PXD005425 | Pride
Project description:GSK3685032-induced DNA hypomethylation results in upregulation of largely viral-responsive gene expression pathways and cell death. We identified that loss of RNF4 causes resistance to GSK3685032. We established RNF4 wild type and deficient MV4-11 cells by CRISPR-Cas9 disruption and treated with vehicle or GSK3685032 to determine how RNF4-deficiency impacts GSK3685032-induced gene expression changes
2026-05-17 | GSE233725 | GEO
Project description:GSK3685032-induced DNA hypomethylation results in upregulation of largely viral-responsive gene expression pathways and cell death. We identified that loss of RNF4 causes resistance to GSK3685032. We established RNF4 wild type and deficient MV4-11 cells by CRISPR-Cas9 disruption and treated with vehicle or GSK3685032 to determine how RNF4-deficiency impacts GSK3685032-induced gene expression changes
2026-05-17 | GSE233722 | GEO
Project description:Metastasis is the deadliest phase of cancer progression. Experimental models using immunodeficient mice have been used to gain insights into the mechanisms of metastasis. We report here the identification of a “metastasis aggressiveness gene expression signature” derived using human melanoma cells selected based on their metastatic potentials in a xenotransplant metastasis model. Comparison with expression data from human melanoma patients shows that this metastasis gene signature correlates with the aggressiveness of melanoma metastases in human patients. Many genes encoding secreted and membrane proteins are included in the signature, suggesting the importance of tumor-microenvironment interactions during metastasis. Keywords: disease state
2007-10-02 | GSE8401 | GEO
Project description:Metastasis is the deadliest phase of cancer progression. Experimental models using immunodeficient mice have been used to gain insights into the mechanisms of metastasis. We report here the identification of a “metastasis aggressiveness gene expression signature” derived using human melanoma cells selected based on their metastatic potentials in a xenotransplant metastasis model. Comparison with expression data from human melanoma patients shows that this metastasis gene signature correlates with the aggressiveness of melanoma metastases in human patients. Many genes encoding secreted and membrane proteins are included in the signature, suggesting the importance of tumor-microenvironment interactions during metastasis. Keywords: disease state analysis
2007-10-02 | GSE7956 | GEO
Project description:Metastasis is the deadliest phase of cancer progression. Experimental models using immunodeficient mice have been used to gain insights into the mechanisms of metastasis. We report here the identification of a “metastasis aggressiveness gene expression signature” derived using human melanoma cells selected based on their metastatic potentials in a xenotransplant metastasis model. Comparison with expression data from human melanoma patients shows that this metastasis gene signature correlates with the aggressiveness of melanoma metastases in human patients. Many genes encoding secreted and membrane proteins are included in the signature, suggesting the importance of tumor-microenvironment interactions during metastasis. Keywords: disease state
2007-10-02 | GSE7929 | GEO