Transcriptomic data from a gallbladder cancer cell line with acquired chemoresistance to gemcitabine [NOZ]
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ABSTRACT:
PROVIDER: PRJNA860574 | ENA |
REPOSITORIES: ENA
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Project description:Gallbladder cancer (GBC) has few therapeutic options, being gemcitabine the first-line chemotherapeutic drug. However, this treatment shows poor clinical outcomes on patients. The acquired resistance phenomenon during of the treatment is one of the main factors that leads to insufficient therapeutic effects, and the molecular mechanisms carried out by tumor cells against gemcitabine are still poorly understood. First, we established a GBC cell line with acquired resistance to gemcitabine (NOZ GemR) from parental cell line (NOZ). After, we used microarray hybridization in NOZ and NOZ GemR to characterize their transcriptional profile to identify differentially expressed genes and/or molecular pathways involved chemoresistant cell phenotype.
2022-07-21 | GSE208659 | GEO
Project description:In order to study the transcriptional changes during the development of gemcitabine resistance in gallbladder cancer cells, we established gemcitabine resistant NOZ cells, named NOZ-R. We then performed RNA sequencing (RNA-seq) to compare transcriptome profiles between NOZ-R and parental NOZ cells.
2026-03-24 | GSE321657 | GEO
Project description:Gallbladder cancer (GBC) has few therapeutic options, being gemcitabine the first-line chemotherapeutic drug. However, this treatment shows poor clinical outcomes on patients. The acquired resistance phenomenon during of the treatment is one of the main factors that leads to insufficient therapeutic effects, and the molecular mechanisms used by tumor cells against gemcitabine are still poorly understood. First, we established a GBC cell line with acquired resistance to gemcitabine (TGBC1 GemR) from parental cell line (TGBC1). After, we used microarray hybridization in TGBC1 and TGBC1 GemR to characterize their transcriptional profile to identify differentially expressed genes and/or molecular pathways involved chemoresistant cell phenotype.
2022-07-21 | GSE208660 | GEO
Project description:Treatment options for advanced gallbladder cancer (GBC) are scarce and usually rely on cytotoxic chemotherapy, but unfortunately the effectiveness of any regimen is limited, and recurrence rates are high. Here, we established and characterized two gemcitabine-resistant GBC cell sublines (NOZ GemR and TGBC1 GemR) to investigate the molecular mechanisms associated with acquired resistance in vitro. The transcriptome profiling of parental and gemcitabine resistant cells revealed differential expression of multiple protein-coding genes and enrichment of biological processes such as epithelial-to-mesenchymal transition and drug metabolism. On the other hand, quantitative phosphotyrosine proteomic analysis of NOZ GemR identified aberrantly dysregulated signaling pathways in resistant cells as well as active kinases, such as Abl, PDGFRA, EphB2 and members of the Src-family that could be novel therapeutic targets against drug resistance in GBC. In line with this, NOZ GemR cells showed increased sensitivity toward the multikinase inhibitor dasatinib compared with parental cells. In conclusion, our study describes transcriptome changes and altered signaling pathways occurring in gemcitabine-resistant gallbladder cancer cells, which greatly expands our understanding of the underlying mechanisms of acquired drug-resistance in GBC. Moreover, this new gemcitabine resistant GBC models could be exploited either to study alternative mechanisms of resistance or to explore new therapies for chemotherapy-refractory GBC.
2023-05-03 | PXD036348 | Pride
Project description:Transcriptomic data from a gallbladder cancer cell line with acquired chemoresistance to gemcitabine [TGBC1]
| PRJNA860575 | ENA
Project description:Liver invasion and metastasis often occur in gallbladder cancer (GBC). We established a liver metastasis mouse model using NOZ cells for two round intrasplenic injection. We acquired a highly metastatic subclone of NOZ cells, we named it LiM2-NOZ(second-round liver metastasis NOZ) cells. Then we characterized the long noncoding RNAs (lncRNAs) and mRNAs that differentially expressed in NOZ and LiM2-NOZ cells.
2017-11-09 | GSE106671 | GEO
Project description:Pancreatic Ductal Adenocarcinoma (PDAC) is associated with extremely poor prognosis due to late diagnosis and therapeutic resistance. Here we show that PDAC cells undergo progressive reprogramming of the global epigenetic landscape during the process of acquiring chemoresistance. Through an epigenetic inhibitor screen, we identified Protein Arginine methyltransferase 1 (PRMT1) as a central driver of chemoresistance in PDAC. Genetic or pharmacological inhibition of PRMT1 impaired adaptive epigenetic reprogramming, sensitized PDAC cells to Gemcitabine and other commonly used chemo drugs, and delayed the development of acquired resistance both in vitro and in vivo. Mechanistically, we find that PRMT1, through its enzymatic activity, limits the accumulation of small bZIP transcription factor MAFF in the nucleus, and the assembly of chromatin-bound MAFF/BACH1 hetero-oligomeric complexes following Gemcitabine treatment. Genetic silencing of MAFF heightened the resistance of PDAC cells to Gemcitabine, and to combination of Gemcitabine and PRMT1 inhibitors. Cut&Tag chromatin profiling of H3K27Ac, MAFF and BACH1 suggests a pivotal role for MAFF/BACH1 in orchestrating global epigenetic reprogramming during the course of acquiring Gemcitabine resistance. Supporting the clinical relevance of our findings, predicted PRMT1 and MAFF/BACH1 genes signatures based on our Cut&Tag analysis were able to distinguish Gemcitabine-resistant from Gemcitabine-sensitive PDAC patient-derived xenografts according to expression changes induced by Gemcitabine. Together, our study reveals a novel epigenetic regulatory axis involving PRMT1 and MAFF/BACH1 that modulates Gemcitabine response, which could be potentially exploited for improving therapeutic response in advanced PDAC.
2024-04-29 | GSE227129 | GEO
Project description:Gemcitabine resistance in gallbladder cancer poses a significant challenge to patient prognosis. This study identified RUVBL2 as a critical factor contributing to gemcitabine resistance in gallbladder cancer. Further analysis, combining ChIP-seq and gene enrichment studies, revealed that RUVBL2 regulates the mitophagy pathway. This regulation helps maintain intracellular redox homeostasis in gallbladder cancer cells following gemcitabine treatment.
2026-01-30 | GSE317548 | GEO
Project description:Poor prognosis in gallbladder cancer is due to late presentation of the disease, lack of reliable biomarkers for early diagnosis and limited targeted therapies. Early diagnostic markers and novel therapeutic targets can significantly improve clinical management of GBC. We carried out quantitative proteomic analysis using a panel of gallbladder cancer cell lines using isobaric tags for relative and absolute quantitation (iTRAQ). We identified 3,655 proteins among which 654 were found to be overexpressed and 387 were downregulated in the invasive cell lines (OCUG-1, NOZ and GB-d1) compared to the non-invasive cell line, TGBC24TKB. Among these, macrophage inhibitory factor (MIF) was observed to be >3-fold overexpressed. MIF is a pleiotropic proinflammatory cytokine that plays a causative role in multiple diseases including cancer. MIF has been reported to play a central role in tumor cell proliferation and invasion in several cancers. Immunohistochemical staining confirmed our findings showing overexpression of MIF in 21 of 29 gallbladder adenocarcinoma cases. A significant decrease in cell viability, colony forming ability and invasive property of the gallbladder cancer cells was observed upon MIF inhibition using MIF siRNA and MIF antagonists. Our findings support the role of MIF in tumor aggressiveness and suggest its potential application as a therapeutic target for gallbladder cancer.
2015-10-02 | PXD001566 | Pride
Project description:Proteins interacting with NSUN2 in gallbladder carcinoma (NOZ cell line)
2019-03-20 | PXD013152 |