Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA93491 | ENA |
REPOSITORIES: ENA
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Project description:The study was done to identify the differentially expressed genes in response to Doxorubicin drug resistance in the 143B human osteosarcoma cell line, using the Microarray technology. Keywords: drug resistance; dual channel; cell line based; doxorubicin resistance; Human osteosarcoma cell line
2007-03-01 | GSE3362 | GEO
Project description:To identify target genes regulated by ALKBH5 in osteosarcoma, we silenced the expression of ALKBH5 in osteosarcoma cell line-143B and tested its effect on 143B transcriptome.
2022-06-28 | GSE154528 | GEO
Project description:In order to understand the effect of FDA-approved drugs including doxorubicin (DOX) and HDACs inhibitors (PXD101 and PCI-24781) on osteosarcoma, 143B osteosarcoma cells were treated with the single agents or combinations of these drugs. Three biological replicates of each sample were processed for next-generation sequencing (NGS).
2025-12-31 | GSE218036 | GEO
Project description:Pulmonary metastasis is the main cause of medical failure and death of osteosarcoma patients. Our recent study identified IRX1 as a potential metastasis-driving gene in osteosarcoma. Studies showed that IRX1 can promote the migration, invasion and anoikis resistance of osteosarcoma cells. We generated 143B stable IRX1 knockdown and control cell lines, and found that IRX1 knockdown can inhibit the pulmonary metastasis of 143B cells in orthotopic mouse osteosarcoma model. Expression microarrays are performed in143B-shCtrl and 143B-shIRX1 cells to study the mechanism of IRX1 on promoting metastasis of osteosarcoma
2015-08-25 | E-GEOD-55958 | biostudies-arrayexpress
Project description:Tumor organoids have emerged as the most promising avatar to model cancer in vitro and to be used as drug testing platform in personalized medicine protocols. The derivation of organoids from epithelial tumors is well established, and their use has proven useful for biomarker discovery, drug screening, and clinical decision support. However, the generation of organoids from sarcomas is much less developed and current protocols require further optimization to fully harness their research and clinical potential. In this study, we explored the challenges of generating basement membrane extract (BME)-based organoids from patient-derived sarcoma samples. Of the 19 samples processed, 3D structures formed in 7 (37%), yet none of these organoids could be propagated beyond the first passage. As an alternative approach, we successfully generated 3D organoids with long-term growth potential from sarcoma xenografts. Of the 14 xenograft samples tested, 7 (50%) could be maintained through at least three passages and were successfully biobanked. Specifically, organoids derived from xenografts grown from parental and doxorubicinresistant 143B osteosarcoma cells could be maintained as long-term cultures and used as a 3D platform to investigate drug resistance in osteosarcoma. Transcriptomic profiling and functional assays performed in these models identified the nonreceptor protein tyrosine kinase SRC as a key mediator of resistance to doxorubicin in osteosarcoma. Importantly, we demonstrated that inhibition of SRC signaling using dasatinib restores doxorubicin sensitivity in osteosarcoma cells by suppressing c-JUN–driven ABCB1 expression.
2026-06-03 | GSE303294 | GEO
Project description:In our study, we found that Siglec-15 was critical to osteosarcoma characteristics. To identify the downstream target genes of Siglec-15 in osteosarcoma, we conducted the RNA-seq analysis of Siglec-15 knockdown in osteosarcoma cell line 143B cells.
2021-05-25 | GSE175414 | GEO
Project description:Pulmonary metastasis is the main cause of medical failure and death of osteosarcoma patients. Our recent study identified IRX1 as a potential metastasis-driving gene in osteosarcoma. Studies showed that IRX1 can promote the migration, invasion and anoikis resistance of osteosarcoma cells. We generated 143B stable IRX1 knockdown and control cell lines, and found that IRX1 knockdown can inhibit the pulmonary metastasis of 143B cells in orthotopic mouse osteosarcoma model.
2015-08-25 | GSE55958 | GEO
Project description:Expression profiling of 143B-shCtrl and 143B-shIRX1 stable osteosarcoma cell lines
| PRJNA241435 | ENA
Project description:Osteosarcoma is the most common type of pediatric bone tumor. Despite great advances in chem-otherapy during the past decades the survival rates of osteosarcoma patients remains usatisfacto-ry. Drug resistance is one of the main reasons leading to treatment failure and poor progno-sis. Previous reports correlated expression of cluster of differentiation 44 (CD44) with drug re-sistance and poor survival of osteosarcoma patients, however the underlying mechanisms are poorly defined. Here, we investigated the role of CD44 in the regulation of drug chemoresistance using osteosarcoma cells isolated from mice carrying a mutation of the tumor suppressor neurofi-bromatosis type 2 (Nf2) gene. CD44 expression was knocked-down in the cells using CRISPR/Cas9 approach. Subsequently, CD44 isoforms and mutants were re-introduced to investigate CD44-dependent processes. Sensitivity to doxorubicin was analyzed in the osteosarcoma cells with modified CD44 expression by immunoblot, colony formation- and WST-1 assay. To dissect the molecular alterations induced by deletion of Cd44, RNA sequencing was performed on Cd44-positive and Cd44-negative primary osteosarcoma tissues isolated from Nf2-mutant mice. Subsequently, expression of candidate genes was evaluated by quantitative reverse transcription PCR (qRT-PCR). Our results indicate that CD44 increases the resistance of osteosarcoma cells to doxorubicin by up-regulating the levels of multidrug resistance (MDR) 1 protein expression, and suggest the role of proteolytically released CD44 intracellular domain, and hyaluronan interac-tions in this process. Moreover, high throughput sequencing analysis identified differential regula-tion of several apoptosis-related genes in Cd44-positive and -negative primary osteosarcomas, in-cluding p53 apoptosis effector related to PMP-22 (Perp). Deletion of CD44 in osteosarcoma cells led to doxorubicin-dependent p53 activation and a profound increase in Perp mRNA expression. Overall, our results suggest that CD44 might be an important regulator of drug resistance and suggest that targeting CD44 can sensitize osteosarcoma to standard chemotherapy.
2022-08-17 | GSE210023 | GEO
Project description:Due to the lack of a precise in vitro model that can mimic the nature microenvironment in osteosarcoma, the understanding of its resistance to chemical drugs remains limited. Here, we report a novel three-dimensional model of osteosarcoma constructed by seeding tumor cells (MG-63 and MNNG/HOS Cl #5) within in demineralized bone matrix scaffolds. Demineralized bone matrix scaffolds retain the original components of the natural bone matrix (hydroxyapatite and collagen type I), and possess good biocompatibility allowing osteosarcoma cells to proliferate and aggregate into clusters within the pores. Growing within the scaffold conferred elevated resistance to doxorubicin on MG-63 and MNNG/HOS Cl #5 cell lines as compared with two-dimensional cultures. Transcriptomic analysis showed an increased enrichment for drug resistance genes along with enhanced glutamine metabolism in osteosarcoma cells in demineralized bone matrix scaffolds. Inhibition of glutamine metabolism resulted a decrease in drug resistance of osteosarcoma, which could be restored by α-ketoglutarate supplementation. Overall, our study suggests that microenvironmental cues in demineralized bone matrix scaffolds can enhance osteosarcoma drug responses and that targeting glutamine metabolism may be a strategy for treating osteosarcoma drug resistance.
2023-12-20 | GSE234632 | GEO