ArticlePloS one2010
Expression of (NES-)hTERT in cancer cells delays cell cycle progression and increases sensitivity to genotoxic stress.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Telomeres, telomerase, and cancer: mechanisms, biomarkers, and therapeutics.Experimental hematology & oncology · 2025Review
- Accumulation of TERT in mitochondria exerts two opposing effects on apoptosis.FEBS open bio · 2023Article
- Establishing and characterizing human stem cells from the apical papilla immortalized by hTERT gene transfer.Frontiers in cell and developmental biology · 2023Article
- Many Functions of Telomerase Components: Certainties, Doubts, and Inconsistencies.International journal of molecular sciences · 2022Review
- Telomerase Biogenesis and Activities from the Perspective of Its Direct Interacting Partners.Cancers · 2020Review
- Telomerase Does Not Improve DNA Repair in Mitochondria upon Stress but Increases MnSOD Protein under Serum-Free Conditions.International journal of molecular sciences · 2019Article
- Mitochondrial Dysfunction in Aging and Cancer.Journal of clinical medicine · 2019Review
- Article
- Antitumor effects of a dual cancer-specific oncolytic adenovirus on colorectal cancerExperimental and therapeutic medicine · 2015Article
- Tissue Specific Promoters in Colorectal Cancer.Disease markers · 2015Review
- Effects of mitochondrial translocation of telomerase on drug resistance in hepatocellular carcinoma cells.Journal of Cancer · 2015Article
- Aging and HIV/AIDS: pathogenetic role of therapeutic side effects.Laboratory investigation; a journal of technical methods and pathology · 2014Review
- Crosstalk between telomere maintenance and radiation effects: A key player in the process of radiation-induced carcinogenesis.Mutation research. Reviews in mutation research · 2014Review
- Mitochondrial telomerase protects cancer cells from nuclear DNA damage and apoptosis.PloS one · 2013Article
- Human telomerase acts as a hTR-independent reverse transcriptase in mitochondria.Nucleic acids research · 2012Article
- Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Telomerase is a reverse transcriptase associated with cellular immortality through telomere maintenance. This enzyme is activated in 90% of human cancers, and inhibitors of telomerase are currently in clinical trials to counteract tumor growth. Many aspects of telomerase biology have been investigated for therapy, particularly inhibition of the enzyme, but little was done regarding its subcellular shuttling. We have recently shown that mutations in the nuclear export signal of hTERT, the catalytic component of telomerase, led to a mutant ((NES-)hTERT) that failed to immortalize cells despite nuclear localization and catalytic activity. Expression of (NES-)hTERT in primary fibroblast resulted in telomere-based premature senescence and mitochondrial dysfunction. Here we show that expression of (NES-)hTERT in LNCaP, SQ20B and HeLa cells rapidly and significantly decreases their proliferation rate and ability to form colonies in soft agar while not interfering with endogenous telomerase activity. The cancer cells showed increased DNA damage at telomeric and extra-telomeric sites, and became sensitive to ionizing radiation and hydrogen peroxide exposures. Our data show that expression of (NES-)hTERT efficiently counteracts cancer cell growth in vitro in at least two different ways, and suggest manipulation with the NES of hTERT or its subcellular shuttling as a new strategy for cancer treatment.
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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.