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Differentiation related tumorigenic potential and transcriptional profile of the fusion reprogrammed mouse cancer cell lines

ABSTRACT: Rebuild tumorgenicity during differentiation of fusion reprogrammed Hepa1-6 cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE30965 | GEO | 2017/02/10

SECONDARY ACCESSION(S): PRJNA146227

REPOSITORIES: GEO

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Tumorigenic potential is restored during differentiation in fusion-reprogrammed cancer cells.

Project description:Detailed understanding of the mechanistic steps underlying tumor initiation and malignant progression is critical for insights of potentially novel therapeutic modalities. Cellular reprogramming is an approach of particular interest because it can provide a means to reset the differentiation state of the cancer cells and to revert these cells to a state of non-malignancy. Here, we investigated the relationship between cellular differentiation and malignant progression by the fusion of four independent mouse cancer cell lines from different tissues, each with differing developmental potentials, to pluripotent mouse embryonic stem (ES) cells. Fusion was accompanied by loss of differentiated properties of the four parental cancer cell lines and concomitant emergence of pluripotency, demonstrating the feasibility to reprogram the malignant and differentiative properties of cancer cells. However, the original malignant and differentiative phenotypes re-emerge upon withdrawal of the fused cells from the embryonic environment in which they were maintained. cDNA array analysis of the malignant hepatoma progression implicated a role for Foxa1, and silencing Foxa1 prevented the re-emergence of malignant and differentiation-associated gene expression. Our findings support the hypothesis that tumor progression results from deregulation of stem cells, and our approach provides a strategy to analyze possible mechanisms in the cancer initiation.

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Fusion Negative Rhabdomyosarcoma Cell Lines

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Project description:BackgroundThe mTOR inhibitor rapamycin has anti-tumor activity across a variety of human cancers, including hepatocellular carcinoma. However, resistance to its growth inhibitory effects is common. We hypothesized that hepatic cell lines with varying rapamycin responsiveness would show common characteristics accounting for resistance to the drug.Methodology/principal findingsWe profiled a total of 13 cell lines for rapamycin-induced growth inhibition. The non-tumorigenic rat liver epithelial cell line WB-F344 was highly sensitive while the tumorigenic WB311 cell line, originally derived from the WB-F344 line, was highly resistant. The other 11 cell lines showed a wide range of sensitivities. Rapamycin induced inhibition of cyclin E-dependent kinase activity in some cell lines, but the ability to do so did not correlate with sensitivity. Inhibition of cyclin E-dependent kinase activity was related to incorporation of p27(Kip1) into cyclin E-containing complexes in some but not all cell lines. Similarly, sensitivity of global protein synthesis to rapamycin did not correlate with its anti-proliferative effect. However, rapamycin potently inhibited phosphorylation of two key substrates, ribosomal protein S6 and 4E-BP1, in all cases, indicating that the locus of rapamycin resistance was downstream from inhibition of mTOR Complex 1. Microarray analysis did not disclose a unifying mechanism for rapamycin resistance, although the glycolytic pathway was downregulated in all four cell lines studied.Conclusions/significanceWe conclude that the mechanisms of rapamycin resistance in hepatic cells involve alterations of signaling downstream from mTOR and that the mechanisms are highly heterogeneous, thus predicting that maintaining or promoting sensitivity will be highly challenging.

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FUSION Cohort Study

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Large scale screening for known fusion genes in cancer cell lines

Project description:We have utilized a version 2.0 of our Fusion gene microarray (version 1.0 described by PMID: 19152679 and GEO, GPL8078) to screen cancer cell lines for known fusion genes We assembled a comprehensive database of published fusion genes, including those which have been reported only in individual studies and samples, and fusion genes resulting from deep sequencing of cancer genomes and transcriptomes. From the total set of 548 fusion genes, we designed 197,846 unique oligonucleotides, targeting both chimeric transcript junctions as well as sequences internal to each of the fusion gene partners. We investigated the presence of fusion genes in a series of 67 cell lines originating from 15 different cancer types. Data from ten leukaemia cell lines with known fusion gene status were used to evaluate and calibrate an automated scoring algorithm. In five out of ten cell lines the correct fusion gene was the top most scoring hit, and one came second, all six passing a cut-off of 50 percent of theoretical maximum-score. Two additional fusion genes, BCAS4-BCAS3 from the MCF-7 breast cancer cell line and CCDC6-RET from the TPC-1 thyroid cancer cell line were validated as true positive fusion transcripts from the remaining 57 cell lines. A total of 67 cell lines from various cancer types were analysed for presence of known fusion genes

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Reprogrammed alveolar macrophages after pneumonia recovery

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Transcription profiling of mouse in vitro reprogrammed fibroblasts carrying retroviral transgenes for Oct4, Sox2, Klf4, and c-Myc to investigate developmental potential

Project description:Comparison of in vitro reprogrammed fibroblasts carrying retroviral transgenes for Oct4, Sox2, Klf4, and c-Myc with non-infected fibroblasts and wt ES cells.

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