ArticleScientific reports2016
Switch telomerase to ALT mechanism by inducing telomeric DNA damages and dysfunction of ATRX and DAXX.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
66 citing papers in PubMed, 88 citations in OpenAlex.
- Article
- Advanced drug delivery platforms targeting cellular senescence: A promising strategy for cancer therapy.Acta pharmaceutica Sinica. B · 2026Review
- Telomeric Ends and Telomerase-Canonical and Non-Canonical Roles in Breast Cancer Tumorigenesis and Therapy Resistance.Biomedicines · 2026Review
- Telomere-driven dysfunctional changes in gynecological cancers: mechanistic insights, biomarker potential, and therapeutic targeting.Frontiers in cell and developmental biology · 2026Review
- Telomerase and alternative lengthening of telomeres coexist in the regenerating zebrafish caudal fins.EMBO reports · 2025Article
- Epitalon increases telomere length in human cell lines through telomerase upregulation or ALT activity.Biogerontology · 2025Article
- Atypical R-loops in cancer: decoding molecular chaos for therapeutic gain.Journal of translational medicine · 2025Review
- CRISPR/Cas technologies in pancreatic cancer research and therapeutics: recent advances and future outlook.Discover oncology · 2025Review
- Applications of CRISPR-Cas9 in mitigating cellular senescence and age-related disease progression.Clinical and experimental medicine · 2025Review
- Telomere function and regulation from mouse models to human ageing and disease.Nature reviews. Molecular cell biology · 2025Review
- Effect of SARS-CoV-2 infection on sperm telomere length.Journal of assisted reproduction and genetics · 2025Article
- Locking the gates of immortality: targeting alternative lengthening of telomeres (ALT) pathways.Medical oncology (Northwood, London, England) · 2025Review
- TERRA and the alternative lengthening of telomeres: a dangerous affair.FEBS letters · 2025Review
- Unveiling the mysteries of extrachromosomal circular DNA: from generation to clinical relevance in human cancers and health.Molecular cancer · 2024Review
- Long Non-Coding RNAs in Neuroblastoma: Pathogenesis, Biomarkers and Therapeutic Targets.International journal of molecular sciences · 2024Review
- BLM helicase unwinds lagging strand substrates to assemble the ALT telomere damage response.Molecular cell · 2024Article
- Molecular Heterogeneity in Leiomyosarcoma and Implications for Personalised Medicine.Current treatment options in oncology · 2024Review
- The Altered Functions of Shelterin Components in ALT Cells.International journal of molecular sciences · 2023Review
- Article
- Cellular senescence in glioma.Journal of neuro-oncology · 2023Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of telomerase or alternative lengthening of telomeres (ALT) is necessary for tumours to escape from dysfunctional telomere-mediated senescence. Anti-telomerase drugs might be effective in suppressing tumour growth in approximately 85-90% of telomerase-positive cancer cells. However, there are still chances for these cells to bypass drug treatment after switching to the ALT mechanism to maintain their telomere integrity. But the mechanism underlying this switch is unknown. In this study, we used telomerase-positive cancer cells (HTC75) to discover the mechanism of the telomerase-ALT switch by inducing telomere-specific DNA damage, alpha-thalassemia X-linked syndrome protein (ATRX) knockdown and deletion of death associated protein (DAXX). Surprisingly, two important ALT hallmarks in the ALT-like HTC75 cells were observed after treatments: ALT-associated promyelocytic leukaemia bodies (APBs) and extrachromosomal circular DNA of telomeric repeats. Moreover, knocking out hTERT by utilizing the CRISPR/Cas9 technique led to telomere elongation in a telomerase-independent manner in ALT-like HTC75 cells. In summary, this is the first report to show that inducing telomeric DNA damage, disrupting the ATRX/DAXX complex and inhibiting telomerase activity in telomerase-positive cancer cells lead to the ALT switch.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.