Transcriptomic Analysis of Gene Networks Regulated by U11 Small Nuclear RNA in Bladder Cancer
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ABSTRACT:
PROVIDER: PRJNA720696 | ENA |
REPOSITORIES: ENA
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Project description:U11 may alter gene expression by affecting the PI3K-Akt signaling pathway and NF-kappa B signaling pathway, regulating alternative splicing events of FN1 and RPL22L1, and ultimately leading to the development of bladder cancer.
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Project description:Small nuclear RNA is a class of non-coding RNA that widely exist in the nucleus of eukaryotes. Accumulated evidences have shown that small nuclear RNAs are associated with the regulation of gene expression in various tumor types. To explore the gene expression changes and its potential effects mediated by U11 snRNA in bladder cancer cells, U11 snRNA knockout and overexpressed cell lines were constructed and further used to analyze the gene expression changes by RNA sequencing. The differentially expressed genes were found to be mainly enriched in tumor-related pathways both in the U11 knockout and overexpression cell lines, such as NF-kappa B signaling pathway, bladder cancer and PI3K-Akt signaling pathway. Furthermore, alternative splicing events were proposed to participate in the potential regulatory mechanism induced by the U11 knockout or overexpression. In conclusion, U11 may be involved in the regulation of gene expression in bladder cancer cells, which may provide a potentially new biomarker for clinical diagnosis and treatment of bladder cancer.
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Project description:Background: Muscle-invasive bladder cancer is a common aggressive disease with unmet clinical needs. Recent work established a set of consensus bladder cancer transcriptomic subtypes that distinguishes the cell identity of bladder cancers for improved diagnosis and treatment. However, how these distinct subtypes are regulated remains unclear. Given the link between super-enhancers and the regulation of cell identity, we hypothesized that epigenetic activation of distinct super-enhancers could drive the transcriptional programs of the various bladder cancer subtypes. Results: Through integrated RNA sequencing and epigenomic profiling of histone marks (H3K27ac, H3K27me3, H3K9me3) in a diverse panel of 15 primary bladder tumours, seven bladder cancer cell lines, and two primary cultures from normal human urothelia, we established the first integrated epigenetic map of bladder cancer and demonstrate the link between bladder cancer subtype and epigenetic control. Through H3K27ac analysis, we identify the repertoire of activated super-enhancers in bladder cancer that distinguish molecular subtypes. Building on these findings, we reveal the super-enhancer-regulated networks of candidate master transcription factors for Luminal and Basal bladder cancer subgroups. We find that FOXA1, a key pioneer factor in Luminal bladder cancers identified in our Luminal transcription factor network, binds subgroup-specific bladder super-enhancers and correlates with their activation. Furthermore, CRISPR-Cas9 inactivating mutation of FOXA1 triggers a shift from Luminal to Basal cell identity. This shift is accompanied by an overexpression of ZBED2, one of the newly identified transcriptional regulators in the Basal-specific transcription factor network. 5Finally, we show that both FOXA1 and ZBED2 play concordant roles in preventing inflammatory response in bladder cancer cells through STAT2 inhibition and promote cancer cell survival. Conclusions: Overall, our study provides new data for understanding epigenetic regulation of muscle- invasive bladder cancer and identifies a coregulated network of super-enhancers and associated transcription factors as new potential targets for the treatment of this aggressive disease
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Project description:Changes in the nuclear positioning of specific genes, depending on their expression status, have been observed in a large diversity of physiological processes. However, gene position is poorly documented in immune cells subjected to activation upon bacterial infection. Using the pig as a model organism, we focused our study on monocytes-derived macrophages and neutrophils, the first lines of defense against pathogens. We examine whether changes in gene expression due to LPS-activation imply genes repositioning in the nuclear space. A transcriptomic analysis was first performed to identify the genes differentially expressed and analyse the networks implicated during LPS-IFNγ activation in monocytes-derived macrophages. This allowed us to select 4 up-regulated (IL1β, IL8, CXCL10 and TNFα) and 4 down-regulated (VIM, LGALS3, TUBA3, and IGF2) genes to be further studied by 3D-FISH for their behavior in the nuclear space, particularly towards their chromosome territories (CT) during macrophages activation. Among the 4 up-regulated genes, 3 changed their position during the activation process while the 4 down-regulated ones did not. The analysis of gene behaviors towards their CT was extended to neutrophils for 3 up- and 2 down-regulated genes and similar results were obtained. Our data suggest that relocation in the nuclear space of genes differentially expressed in activated immune cells is gene specific and concern mostly up-regulated ones. Porcine monocyte-derived macrophages: Control vs. LPS-IFNγ activated vs. T-2 toxin/LPS-IFNγ activated. A common reference hybridization scheme was used to compare the three-condition experiment, CM vs. AM vs. TAM. The reference consisted of a pool of RNA from all samples. Biological replicates: 5 control, 5 LPS-IFNγ activated, 5 T-2 toxin/LPS-IFNγ activated independently. One replicate per array.
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Project description:The activation status of some DNA damage repair proteins is closely related to the efficacy of CDDP chemotherapy in MIBC. In this study, we used CRISPR/cas9 gene-editing technology to construct hMSH2-deficient bladder cancer cells and confirmed that loss of hMSH2 decreased the sensitivity of bladder cancer cells to cisplatin. Transcriptome analysis was performed to find the potential genes that could be regulated by hMSH2.
2024-06-20 | GSE193754 | GEO
Project description:Background: Muscle-invasive bladder cancer is a common aggressive disease with unmet clinical needs. Recent work established a set of consensus bladder cancer transcriptomic subtypes that distinguishes the cell identity of bladder cancers for improved diagnosis and treatment. However, how these distinct subtypes are regulated remains unclear. Given the link between super-enhancers and the regulation of cell identity, we hypothesized that epigenetic activation of distinct super-enhancers could drive the transcriptional programs of the various bladder cancer subtypes. Results: Through integrated RNA sequencing and epigenomic profiling of histone marks (H3K27ac, H3K27me3, H3K9me3) in a diverse panel of 15 primary bladder tumours, seven bladder cancer cell lines, and two primary cultures from normal human urothelia, we established the first integrated epigenetic map of bladder cancer and demonstrate the link between bladder cancer subtype and epigenetic control. Through H3K27ac analysis, we identify the repertoire of activated super-enhancers in bladder cancer that distinguish molecular subtypes. Building on these findings, we reveal the super-enhancer-regulated networks of candidate master transcription factors for Luminal and Basal bladder cancer subgroups. We find that FOXA1, a key pioneer factor in Luminal bladder cancers identified in our Luminal transcription factor network, binds subgroup-specific bladder super-enhancers and correlates with their activation. Furthermore, CRISPR-Cas9 inactivating mutation of FOXA1 triggers a shift from Luminal to Basal cell identity. This shift is accompanied by an overexpression of ZBED2, one of the newly identified transcriptional regulators in the Basal-specific transcription factor network. 5Finally, we show that both FOXA1 and ZBED2 play concordant roles in preventing inflammatory response in bladder cancer cells through STAT2 inhibition and promote cancer cell survival. Conclusions: Overall, our study provides new data for understanding epigenetic regulation of muscle- invasive bladder cancer and identifies a coregulated network of super-enhancers and associated transcription factors as new potential targets for the treatment of this aggressive disease
2024-05-23 | GSE195768 | GEO
Project description:The activation status of some DNA damage repair proteins is closely related to the efficacy of CDDP chemotherapy in MIBC. In this study, we used CRISPR/cas9 gene-editing technology to construct hMSH2-deficient bladder cancer cells and confirmed that loss of hMSH2 decreased the sensitivity of bladder cancer cells to cisplatin. Transcriptome analysis was performed to find the potential genes that could be regulated by hMSH2.
2024-06-20 | GSE193753 | GEO