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Genome-wide CRISPR screening using cell lines that harbor the mutant hTERT-CRISPR allele.

ABSTRACT: To assess the biological significances of p-hTERT in ALT cells, we used the CRISPR-Cas9 system targeting the hTERT gene and performed genome-wide CRISPR screening, which identified genes in the Fanconi anemia/BRCA pathway as synthetic lethal partners of hTERT.

ORGANISM(S): Homo sapiens

PROVIDER: GSE226994 | GEO | 2024/04/08

REPOSITORIES: GEO

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Transcriptome data from U2OS cells and hTERT CRISPR clones

Project description:To assess the biological significances of p-hTERT in ALT cells, we used the CRISPR-Cas9 system targeting the hTERT gene and performed RNA-seq to analyze the profile of gene expression in hTERT-CRISPR clones (clone#1 and #2). The subsequent gene ontology (GO) analysis showed enrichment of genes involved in cell cycle process and DNA replication within genes down-regulated in hTERT-CRISPR clones.

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TCEAL7 Inhibition of c-Myc Activity in Alternative Lengthening of Telomeres Regulates hTERT Expression

Project description:Replicative senescence forms a major barrier to tumor progression. Cancer cells bypass this by using one of the two known telomere maintenance mechanisms: telomerase or the recombination-based alternative lengthening of telomeres (ALT) mechanism. The molecular details of ALT are currently poorly understood. We have previously shown that telomerase is actively repressed through complex networks of kinase, gene expression, and chromatin regulation. In this study, we aimed to gain further understanding of the role of kinases in the regulation of telomerase expression in ALT cells. Using a whole human kinome siRNA screen, we highlighted 106 kinases whose expression is linked to hTERT promoter activity. Network modeling of transcriptional regulation implicated c-Myc as a key regulator of the 106 kinase hits. Given our previous observations of lower c-Myc activity in ALT cells, we further explored its potential to regulate telomerase expression in ALT. We found increased c-Myc binding at the hTERT promoter in telomerase-positive compared with ALT cells, although no expression differences in c-Myc, Mad, or Max were observed between ALT and telomerase-positive cells that could explain decreased c-Myc activity in ALT. Instead, we found increased expression of the c-Myc competitive inhibitor TCEAL7 in ALT cells and tumors and that alteration of TCEAL7 expression levels in ALT and telomerase-positive cells affects hTERT expression. Lower c-Myc activity in ALT may therefore be obtained through TCEAL7 regulation. Thus, TCEAL7 may present an interesting novel target for cancer therapy, which warrants further investigation.

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A gene expression signature classifying telomerase and ALT immortalization II

Project description:A gene expression signature classifying telomerase and ALT immortalisation reveals an hTERT regulatory network and suggests a mesenchymal stem cell origin for ALT Telomere length is maintained by 2 known mechanisms, activation of telomerase or alternative lengthening of telomeres (ALT). The molecular mechanisms regulating the ALT phenotype are poorly understood and it is unknown how the decision of which pathway to activate is made at the cellular level. We have shown previously that active repression of telomerase gene expression by chromatin remodelling of the promoters is one mechanism of regulation, however other genes and signalling networks are likely to be required to regulate telomerase and maintain the ALT phenotype. Using gene expression profiling we have uncovered a signature of 1305 genes to distinguish telomerase positive and ALT cell lines. By combining this with gene expression profiles of liposarcoma tissue samples we refined this signature to 297 genes significantly associated with telomere maintenance mechanism. Network analysis of known direct interactions between genes within this signature revealed a regulatory signalling network consistent with a model of hTERT repression in ALT cell lines and liposarcomas. This network expands on our existing knowledge of hTERT regulation and provides a platform to understand differential regulation of hTERT in different tumour types and normal tissues. In addition we show evidence to suggest a novel mesenchymal stem cell origin for ALT immortalisation in cell lines and mesenchymal tissues. Keywords: cell type comparison, gene expression

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A gene expression signature classifying telomerase and ALT immortalization I

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Human gastric mucosa: 3 paired hTERT-negative para cancerous tissue (Control) vs. hTERT-positive gastric cancer tissue

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Project description:To investigate the function of p-hTERT in nuclear speckles, we isolated hTERT complex by immunoprecipitation with an anti-hTERT mAb from nuclear speckles purified biochemically and conducted RIP-seq analysis for RNAs associated with hTERT in nuclear speckles.

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