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Gene expression in Trp53 and Rb1 double knockout mouse prostate epithelial cancer cells expressing PIM1

ABSTRACT: Gene expression in Trp53 and Rb1 double knockout mouse prostate epithelial cancer cells expressing PIM1

PROVIDER: PRJNA486800 | ENA |

REPOSITORIES: ENA

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Gene expression in Trp53 and Rb1 double knockout mouse prostate epithelial cancer cells expressing PIM1

Project description:To identify the downstream molecules that mediate PIM1 induced aggressive prostate cancer cells, p53 and Rb-deficient mouse prostate epithelial cells were transduced with PIM1 lentivirus and performed a gene expression profile microarray.

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Transcriptome profiles of control and PIM1 over-expressing LNCaP cells in complete media

Project description:We used control and PIM1 over-expressing LNCaP cells to analyze the effect of PIM1 on gene expression. We find that PIM1 over-expression results in up- and down-regulation of different classes of genes, including increasing gene expression involved in extracellular matrix organization, cell adhesion, and cytokine signaling.

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RNAi profiling of human cells with MYC or PIM1 silencing

Project description:It has been estimated that about 11% of cellular genes present a functional E box to which MYC can associate on the genome. MYC silencing demonstrated that MYC recruits PIM1 at specific MYC binding sites and confocal microscopy following growth factor treatment, showed an elevated degree of nuclear co-localization of PIM1 with nascent transcripts and with MYC suggesting that PIM1 is recruited by MYC to a large number of sites. To understand the actual extension of PIM1 and MYC co-operation in gene transcription we performed expression profile analysis of 293 cells silenced either for MYC or PIM1 at 120 minutes after serum treatment. MYC silencing affected the expression of 1026 genes of which 818 were up-regulated and 208 were down-regulated. Comparison of genes regulated by MYC with those regulated by PIM1, by RNAi silencing, showed that PIM1 contributes to the regulation of 207 genes out of the 1026 MYC-regulated genes. Thus, a subset of 20% of MYC-regulated genes, are also regulated by PIM1. The co-regulated includes genes involved in cell metabolism, protein synthesis, cycle progression, and oncogenesis. Interestingly, a large number of genes are transcriptional factors, which suggests that PIM1 participates in MYC-dependent regulatory networks. Experiment Overall Design: The gene expression analysis was performed by hybridizing RNA samples to the Whole Human Genome Oligo Microarray from Agilent Technologies. Samples were obtained from 293 cells, treated with serum for 120 minutes, expressing either two independent MYC shRNA (shMYC#1 and shMYC#2) or their relative scrambled shRNA (shsM#1 and shsM#2) for MYC expression analysis; two independent PIM1 shRNA (shPIM1#1 and shPIM1#2) or their relative scrambled shRNA (shsP#1 and shsP#2) for PIM1 expression analysis.

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Loss of Pim1 Imposes a Hyperadhesive Phenotype on Endothelial Cells

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Project description:T cell antigen-receptor (TCR) and cytokine receptor engagement trigger large changes in Serine/Threonine kinase signalling networks to drive T cell activation and differentiation. The role of only few kinase signalling pathways have been studied in detail, and in this context, Pim kinases are an interesting, yet understudied, family of Serine/Threonine kinases, with reported roles in key processes including survival, proliferation, metabolism across a range of cell types. T lymphocytes predominantly express PIM1 and PIM2, which are rapidly induced by TCR, costimulation and cytokine signalling. Using high-resolution mass spectrometry we systematically examine the impact of Pim1/Pim2 double deficiency downstream of initial TCR engagement. We find that Pim kinases are dispensable for TCR-driven T cell activation and have little impact on the total proteome in these cells.

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Effect of Trp53 and Rb1 knockout and Myc overexpression on fallopian tube epithelial organoids

Project description:Effect of Trp53 and Rb1 knockout and Myc overexpression on fallopian tube epithelial organoids

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