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Transcriptomic data from a gallbladder cancer cell line with acquired chemoresistance to gemcitabine [TGBC1]

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE208660 | GEO | 2022/07/21

REPOSITORIES: GEO

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Transcriptomic data from a gallbladder cancer cell line with acquired chemoresistance to gemcitabine [NOZ]

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.

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Transcriptome and phosphoproteome analyses of gemcitabine-resistant gallbladder cancer cells provide novel insights into molecular changes occurring during acquired resistance

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

Transcriptomic data from a gallbladder cancer cell line with acquired chemoresistance to gemcitabine [TGBC1]

Project description:Transcriptomic data from a gallbladder cancer cell line with acquired chemoresistance to gemcitabine [TGBC1]

| PRJNA860575 | ENA

Transcriptomic data from a gallbladder cancer cell line with acquired chemoresistance to gemcitabine [NOZ]

Project description:Transcriptomic data from a gallbladder cancer cell line with acquired chemoresistance to gemcitabine [NOZ]

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RNA sequencing revealed the multi-stage transcriptome transformations during the development of gallbladder cancer associated with chronic inflammation

Project description:Purpose Gallbladder cancer (GBC) is a highly malignant tumor with extremely poor prognosis. Previous studies have suggested that the carcinogenesis and progression of GBC is a multi-stage and multi-step process, but most of them focused on the genome changes. And a few studies just compared the transcriptome differences between tumor tissues and adjacent noncancerous tissues. The transcriptome changes, relating to every stage of GBC evolution, have rarely been studied. Methods We selected three cases of normal gallbladder, four cases of gallbladder with chronic inflammation induced by gallstones, five cases of early GBC, and five cases of advanced GBC, using next-generation RNA sequencing to reveal the changes in mRNAs and lncRNAs expression during the evolution of GBC. Results In-depth analysis of the sequencing data indicated that transcriptome changes from normal gallbladder to gallbladder with chronic inflammation were distinctly related to inflammation, lipid metabolism, and sex hormone metabolism; transcriptome changes from gallbladder with chronic inflammation to early GBC were distinctly related to immune activities and connection between cells; and the transcriptome changes from early GBC to advanced GBC were distinctly related to transmembrane transport of substances and migration of cells. Conclusion Expression profiles of mRNAs and lncRNAs change significantly during the evolution of GBC, in which lipid-based metabolic abnormalities play an important promotive role, inflammation and immune activities play a key role, and changes in membrane proteins are the most highlighted molecular changes.

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CEACAM6 orchestrates gallbladder cancer aggressiveness through molecular interplay with Integrin and PRKCD [SNU308]

Project description:Gallbladder cancer (GBC) comprises the most common biliary tract cancer (BTC). However, GBC is a rare disease often manifesting as aggressive malignancy due to its late diagnosis and resistance to chemotherapy. The identification of molecular drivers of GBC and identification of targeted therapies is still urgently needed. This study combined proteomic analysis of GBC patient samples, functional and molecular characterization of potential oncogenes, and identification of potential therapy strategy for GBC. We identified Carcinoembryonic Antigen-related Cell Adhesion Molecule 6 (CEACAM6) as one of the strongest and most significant upregulated proteins in GBC samples. Functional analysis and in vivo mouse models revealed that CEACAM6 supported the initial steps of cancer metastasis by decreasing cell adhesion while promoting migration and invasion of GBC cells. BirA-BioID followed by mass-spectrometry revealed Integrin Beta-1 (ITGB1) and Protein Kinase C Delta (PRKCD) as direct molecular and functional partners of CEACAM6 in supporting GBC cell migration through regulation of ERK and AKT downstream target genes MMP13, MMP14, and OCLN. Conversely, CEACAM6 knockdown abolished GBC aggressiveness, and treatment using AKT inhibitor Capivasertib and ERK inhibitor Ulixertinib counter-acted the CEACAM6-induced migration.These findings demonstrate that CEACAM6 is crucial for gallbladder oncogenesis through ERK and AKT signaling, providing insights into the design of therapeutic strategies for GBC.

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CEACAM6 orchestrates gallbladder cancer aggressiveness through molecular interplay with Integrin and PRKCD [GB-d1]

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Gene expression signatures of highly metastatic gallbladder cancer cells

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

miRNA profiling in gallbladder carcinoma

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Expression data from gemcitabine treated pancreatic CAFs

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2016-03-09 | E-GEOD-78982 | biostudies-arrayexpress

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