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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Alternative Lengthening of Telomeres (ALT) and ATRX inactivation in high grade pediatric osteosarcomas

ABSTRACT: DNA microarrays were used to define the transcriptional profiles of tumor samples to compare 12 high-grade pediatric osteosarcoma tumor samples on their ALT and ATRX status.

ORGANISM(S): Homo sapiens

SUBMITTER: Pascal Finetti

PROVIDER: E-MTAB-11743 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Signalling Inhibition by Ponatinib Disrupts Productive Alternative Lengthening of Telomeres (ALT)

Project description:Alternative lengthening of telomeres (ALT) supports telomere maintenance and replicative immortality in around 10-15% of cancers, thus representing a compelling target for therapy.To identify anti-cancer drugs that can be repurposed as ALT-centered therapies, we performed for a compound library screen on isogenic cell lines that rely either on telomerase or ALT mechanisms. We validated candidates on a panel of ALT- vs. telomerase-positive sarcoma cells and assessed levels of extrachromosomal telomeric C-circles after drug treatment, as a bona fide marker of ALT activity. We identified a receptor tyrosine kinase inhibitor ponatinib that deregulated ALT mechanisms, increased telomeric replicative stress and induced telomeric dysfunction in ALT cells. Using a model of ALT sarcoma xenografts, we found that ponatinib targeted ALT-positive cells and mitigated telomere elongation in these tumors. To identify the mode of action of ponatinib on ALT, we performed RNA-sequencing and quantitative proteomic and phosphoproteomic analyses, and shortlisted candidates to test the effect of their loss on telomeric C-circle levels. We identified an ABL1-JNK-JUN signalling circuit to be inhibited by ponatinib and to have a role in suppressing extrachromosomal telomeric C-circle formation. Furthermore, transcriptome and interactome analyses of JUN suggested a role of JUN in DNA damage repair pathways, independently of its capacity as a transcription factor. These results were corroborated by new synergistic drug interactions between ponatinib and either DNA synthesis or repair inhibitors such as triciribine and KU-60019, respectively. Overall, we identified a novel signalling pathway impacting ALT which can be targeted by a clinically approved kinase inhibitor.

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