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MicroRNAseq of primary human gallbladder cells, reprogrammed human gallbladder cells, and human pancreatic beta cells

ABSTRACT: We determined the global microRNA expression profiles of primary human gallbladder cells and genetically reprogrammed human gallbladder cells and compared with pancreatic beta cells to ascertain the degree of cellular transdifferentatiation of insulin-producing human gallbladder cells to become beta-like cells. First, we cultured patient-derived gallbladder cells and then we transduced these with beta cell transcription factors to reprogram gallbladder cells to become beta-like cells. We used a pan-islet surface monoclonal antibody to enrich for insulin-producing reprogrammed human gallbladder cells using FACS.

INSTRUMENT(S): Illumina HiSeq 2500, Illumina HiSeq 2000

ORGANISM(S): Homo sapiens

SUBMITTER: Jonathan Schug

PROVIDER: E-MTAB-5554 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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RNAseq of primary human gallbladder cells, reprogrammed human gallbladder cells, and human pancreatic beta cells

Project description:We determined the global gene expression profiles of primary human gallbladder cells and genetically reprogrammed human gallbladder cells and compared with pancreatic beta cells to ascertain the degree of cellular transdifferentatiation of insulin-producing human gallbladder cells to become beta-like cells. First, we cultured patient-derived gallbladder cells and then we transduced these with beta cell transcription factors to reprogram gallbladder cells to become beta-like cells. We used a pan-islet surface monoclonal antibody to enrich for insulin-producing reprogrammed human gallbladder cells using FACS.

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microRNAseq of primary human gallbladder cells, reprogrammed human gallbladder cells, and human pancreatic beta cells

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RNAseq of primary human gallbladder cells, reprogrammed human gallbladder cells, and human pancreatic beta cells

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Project description:We report here an improved protocol to reprogram mouse gallbladder cells (GBCs) into pancreatic beta cells. To fully understand the extent of reprogramming, mRNA was extracted from FACS-purified MIP-GFP positive insulin-producing cells (namely rGBC2) for RNA-seq after 10-days of in vitro reprogramming. The global gene expression profile of rGBC2 was compared with that of primary gallbladder cells, GBC reprogrammed with the rGBC1 protocol (Hickey et al., 2013) and mouse pancreatic β cells (Benner et al., 2014). We show that rGBC2 from four independent cell batches showed a unique gene expression phenotype. Compared with the rGBC1 protocol, rGBC2 expressed many additional pancreatic β cell genes, suppressed many gallbladder genes and resulted in an expression profile closer to pancreatic β cells.

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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.

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R-spondin 1 and noggin facilitate expansion of resident stem cells from non-damaged gallbladders.

Project description:Pioneering studies within the last few years have allowed the in vitro expansion of tissue-specific adult stem cells from a variety of endoderm-derived organs, including the stomach, small intestine and colon. Here we derived organoids from mouse gallbladder tissue (gallbladder organoids), from mouse liver (including the extrahepatic biliary ducts and gallbladder; liver organoids) and from mouse small intestine tissue (intestinal organoids). RNA was prepared from these organoids and used to assay expression of 21,258 genes using Affymetrix gene expression arrays. RNA was also prepared from mouse gallbladder, liver and small intestine tissues and used to assay gene expression in these tissues. Finally, gallbladder organoids were induced to differentiate by removing R-spondin 1 and noggin from the culture media and subjected to gene expression array analysis. RNA was extracted from mouse gallbladder organoids, differentiated gallbladder organoids, liver organoids, small intestine organoids, gallbladder tissue, liver tissue and small intestine tissue and then used for hybridization of Affymetrix gene expression microarrays.

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Identification of circulating lncRNAs associated with gallbladder cancer risk by tissue-based preselection, cis-eQTL validation, and analysis of association with genotype-based expression

Project description:Long non-coding RNAs (lncRNAs) play key roles in cell processes and are good candidates for cancer risk prediction. Few studies have investigated the association between individual genotypes and lncRNA expression. Here we integrate three separate datasets with information on lncRNA expression only, both lncRNA expression and genotype, and genotype information only, to identify circulating lncRNAs associated with the risk of gallbladder cancer (GBC), using robust linear and logistic regression techniques. In the first dataset, we preselect lncRNAs based on expression changes along the sequence “gallstones → dysplasia → GBC”. In the second dataset, we validate associations between genetic variants and serum expression levels of the preselected lncRNAs (cis-lncRNA-eQTLs) and build lncRNA-expression prediction models. In the third dataset, we predict serum lncRNA expression based on individual genotypes, and assess the association between genotype-based expression and GBC risk. AC084082.3 and LINC00662 showed increasing expression levels (p value = 0.009), while C22orf34 expression decreased in the sequence from gallstones to GBC (p value = 0.04). We identified and validated two cis-LINC00662-eQTLs (r2= 0.26) and three cis-C22orf34-eQTLs (r2 = 0.24). Only LINC00662 showed a genotyped-based serum expression associated with GBC risk (OR=1.25 per log2 expression unit, 95%CI 1.04-1.52, p value = 0.02).

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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.

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