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Extralchromosomal telomere repeat DNA activates cytosolic DNA sensing pathway and influences ALT development
Extrachromosomal telomere repeat (ECTR) DNA is unique to cancer cells that maintain telomeres through the alternative lengthening of telomeres (ALT) pathway, but the role of ECTRs in ALT development remains elusive, until now.

A recent study at the Institute of Molecular Biology, Academia Sinica discovered that extra-chromosomal telomere repeat (ECTR) DNA molecules can activate cytosolic DNA sensing pathways that may inhibit alternative lengthening of telomeres (ALT) cancer development. Results from this study was published online in Nature Structural and Molecular Biology on 6 November 2017.

ALT is a homologous recombination-mediated telomere elongation mechanism implicated in 10-15% types of cancer. ECTR DNA molecules are generated during ALT development and are abundant in ALT cancer cells. However, whether ECTRs play a role in ALT development remains elusive.

Research conducted by Dr. Liuh-Yow Chen鈥檚 lab investigates the development process of ALT-associated cancers to shed light in regard to treatment possibilities. Results from this recent study demonstrates that the ECTR generation that is associated with ALT development may affect tumorigenesis by activating the STING-mediated pathway. Although ECTRs are present in the cytoplasm, the cellular DNA sensing mechanism that reacts to ECTRs is commonly defective in ALT cancer cells.

In contrast, upon induction in the control group of human fibroblasts, ECTRs activate the cGAS-STING-TBK1-IRF3 signaling axis to induce IFN production and thus trigger a type I interferon response, which consequently causes an inhibitory effect on cell proliferation.

Dr. Chen鈥檚 lab further found that the STING expression is also inhibited in ALT cancer cell lines and transforms ALT cell strands. Intriguingly, the ALT-associated tumor suppressors ATRX/Daxx histone chaperon complex and histone H3.3 are also required for activation of this DNA sensing pathway. Co-expression of STING and ATRX in ALT cancer cells reconstitute the DNA sensing mechanism.

Collectively, this study reveals that the loss of the DNA sensing pathway may be a prerequisite for evading ECTR-induced anti-proliferation effects, which then permits ALT development. The key role of this DNA sensing pathway may be further explored and utilized for treatments specific to ALT cancer.

The work in Dr. Chen鈥檚 lab has been supported by the Career Development Award from Academia Sinica and grants from the Ministry of Science and Technology, Taiwan.

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