Essential role of JAB1 in human chondrosarcoma pathogenesis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA566202 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10832081.fastq.gz | Fastqsanger.gz | |||
| SRR10832082.fastq.gz | Fastqsanger.gz | |||
| SRR10832083.fastq.gz | Fastqsanger.gz | |||
| SRR10832084.fastq.gz | Fastqsanger.gz | |||
| SRR10832085.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
Similar Datasets
Project description:JAB1 is a regulator of ubiquitin mediated protein degradation upstream of the 26S proteasome. JAB1 regulates the ubiquitin proteasome system through controlling the activity of the largest family of E3 ubiquitin ligases, the Cullin-RING Ligases. JAB1 is also a transcriptional co-factor contolling the expression of numerous genes and regulates musculoskeletal development in vivo. It is reported that JAB1 is overexpressed in many cancers, making it a potential oncogene. Thus, JAB1 has a highly spatiotemporal specific role in development and cancer pathogenesis. This study aims to determine the JAB1-mediated transcriptome that exists in osteosarcoma cells.
2020-06-10 | GSE117773 | GEO
Project description:Essential role of Jab1 in mouse chondrocyte differentiation.
| PRJNA599392 | ENA
Project description:The p53-dependent role of JAB1 in OS pathogenesis
| PRJNA483169 | ENA
Project description:RNA sequencing was performed at the Genomics Core - Case Western Reserve University
2021-11-18 | GSE137683 | GEO
Project description:Chondrosarcoma is the second most common type of bone cancer. At present, the most effective clinical course of action is surgical resection. Cisplatin is the chemotherapeutic medication most widely used for the treatment of chondrosarcoma; however, its effectiveness is severely hampered by drug resistance. In the current study, we compared cisplatin-resistant chondrosarcoma SW1353 cells with their parental cells via RNA sequencing. Our analysis revealed that glutamine metabolism is highly activated in resistant cells but glucose metabolism is not. Amphiregulin (AR), a ligand of the epidermal growth factor receptor, enhances glutamine metabolism and supports cisplatin resistance in human chondrosarcoma by promoting NADPH production and inhibiting ROS accumulation. The MEK, ERK, and NrF2 signaling pathways were shown to regulate AR-mediated SLC1A5 and GLS expression as well as glutamine metabolism in cisplatin-resistant chondrosarcoma. The knockdown of AR expression in cisplatin-resistant chondrosarcoma cells was shown to reduce the expression of SLC1A5 and GLS in vivo. These results indicate that AR and glutamine metabolism are worth pursuing as therapeutic targets in dealing with cisplatin-resistant human chondrosarcoma.
2023-08-07 | GSE239911 | GEO
Project description:Cellular differentiation and lineage commitment are considered to be robust and irreversible processes during development. Recent work has shown that mouse and human fibroblasts can be reprogrammed to a pluripotent state with a combination of four transcription factors. This raised the question of whether transcription factors could directly specify somatic cell fates in cells such as pancreatic ? cells, contractile cardiomyocytes and neurons. We hypothesized that combinatorial expression of chondrocyte-specific transcription factors could directly convert human amnion cells into chondrosarcoma. Starting from a pool of candidate genes, we identified a combination of only five genes (5F pool), BCL6, T (also called BRACHYURY), c-MYC, MITF and BAF60C (also called SMARCD3) that rapidly and efficiently convert postnatal human amnion into chondrosarcoma. The cells generated expressed multiple cartilage-specific genes such as collagen type II ?1, link protein-1 and aggrecan, and exhibited characteristics of cartilage both in vivo and in vitro. Expression of the endogenous genes for T and MITF was initiated, implying that the cell conversion is due to not only the forced expression of the transgenes, but also the cellular reprogramming by the transgenes. The same set of genes converted human placental artery-derived endothelial (hPAE) cells and menstrual blood-derived cells into chondrosarcoma cells, implying that this conversion is independent of cell types. Direct conversion system from non-cartilage tissue to cartilaginous tissue contributes substantially to a major advance toward cartilage development, oncogenesis of chondrocytes, and cell-based therapy. We hypothesized that combinatorial expression of chondrocyte-specific transcription factors could directly convert human amnion cells into chondrosarcoma. Starting from a pool of candidate genes, we identified a combination of only five genes that rapidly efficiently convert postnatal human amnion into chondrosarcoma.
2011-06-07 | E-GEOD-29745 | biostudies-arrayexpress
Project description:Cellular differentiation and lineage commitment are considered to be robust and irreversible processes during development. Recent work has shown that mouse and human fibroblasts can be reprogrammed to a pluripotent state with a combination of four transcription factors. This raised the question of whether transcription factors could directly specify somatic cell fates in cells such as pancreatic β cells, contractile cardiomyocytes and neurons. We hypothesized that combinatorial expression of chondrocyte-specific transcription factors could directly convert human amnion cells into chondrosarcoma. Starting from a pool of candidate genes, we identified a combination of only five genes (5F pool), BCL6, T (also called BRACHYURY), c-MYC, MITF and BAF60C (also called SMARCD3) that rapidly and efficiently convert postnatal human amnion into chondrosarcoma. The cells generated expressed multiple cartilage-specific genes such as collagen type II α1, link protein-1 and aggrecan, and exhibited characteristics of cartilage both in vivo and in vitro. Expression of the endogenous genes for T and MITF was initiated, implying that the cell conversion is due to not only the forced expression of the transgenes, but also the cellular reprogramming by the transgenes. The same set of genes converted human placental artery-derived endothelial (hPAE) cells and menstrual blood-derived cells into chondrosarcoma cells, implying that this conversion is independent of cell types. Direct conversion system from non-cartilage tissue to cartilaginous tissue contributes substantially to a major advance toward cartilage development, oncogenesis of chondrocytes, and cell-based therapy.
2011-06-07 | GSE29745 | GEO
Project description:microRNAs are small (22-24 nucleotide), non-coding RNA transcripts that play a role in RNA silencing and post transcriptional regulation of gene expression. They have been implicated to have profound roles in many cancers. The role of microRNAs in chondrosarcoma progression is not well understood. Our lab has identified miR-181a to be up-regulated in chondrosarcoma. miR-181a modulates CXCR4 signaling by targeting RGS-16, leading to increased levels of VEGF and MMP-1, major factors in tumor invasion. In an effort to identify other targets of miR-181a apart from RGS-16, we carried out a gene array to compare gene expression between untreated/control CS-1(chondrosarcoma cell line) cells and CS-1 cells transduced with a lenti virus expression construct with anti-miR-181a sequence.
2018-06-19 | GSE70065 | GEO
Project description:Transcriptional profiling of human chondrosarcoma sphere vs adherent cells
2015-04-30 | GSE47823 | GEO
Project description:These libraries represent instances of Swarm rat chondrosarcoma tumors taken from different transplantation experiments. This series also contains one non-cancerous cartilage library made from rat normal growing femoral head cartilage as a comparative data point. Keywords: other
2004-07-24 | GSE1517 | GEO