ArticleMolecular and cellular biology2006
Induction of nitric oxide synthase-dependent telomere shortening after functional inhibition of Hsp90 in human tumor cells.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 38 citations in OpenAlex.
- Redox regulation of telomerase and telomeres in cancer: a critical appraisal of exposure, causality and molecular directness.Molecular biology reports · 2026Review
- Causal Inference Approaches Reveal Associations Between LDL Oxidation, NO Metabolism, Telomere Length and DNA Integrity Within the MARK-AGE Study.Antioxidants (Basel, Switzerland) · 2025Article
- Heat shock proteins as hallmarks of cancer: insights from molecular mechanisms to therapeutic strategies.Journal of hematology & oncology · 2024Review
- The Telomere-Telomerase System Is Detrimental to Health at High-Altitude.International journal of environmental research and public health · 2023Article
- Human telomerase inhibitors from microbial source.World journal of microbiology & biotechnology · 2015Review
- The HSP90 inhibitor alvespimycin enhances the potency of telomerase inhibition by imetelstat in human osteosarcoma.Cancer biology & therapy · 2015Article
- Understanding the role of heat shock protein isoforms in male fertility, aging and apoptosis.The world journal of men's health · 2014Review
- Expression of endothelial nitric oxide synthase protein is not necessary for mechanical strain-induced nitric oxide production by cultured osteoblasts.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2012Article
- Hsp90 modulates CAG repeat instability in human cells.Cell stress & chaperones · 2010Article
- Targeting the dynamic HSP90 complex in cancer.Nature reviews. Cancer · 2010Review
- Heat shock proteins: essential proteins for apoptosis regulation.Journal of cellular and molecular medicine · 2008Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
In most cancer cells, the lengths of telomeres, the functional DNA-protein complexes located at chromosome ends, are maintained by the ribonucleoprotein telomerase. Hsp90 facilitates the assembly of telomerase and remains associated with the functional complex, implying a direct involvement of Hsp90 in telomere length regulation. In an effort to elucidate the effects of Hsp90 inhibition on function and viability of human prostate cancer cells, both pharmacological (radicicol) and genetic (small interfering RNA) approaches were utilized to target Hsp90. Depletion of functional Hsp90 caused dramatic telomere shortening followed by apoptosis. Of particular significance, these cells exhibit a high level of nitric oxide synthase (NOS)-dependent free radical production, and simultaneous treatment of cells with the NOS inhibitor L-NAME resulted in telomere elongation and prevention of apoptosis. In addition, we observe significant DNA damage assessed by telomere dysfunction, although in the absence of a classical DNA damage response. Overall, our data suggest a novel mechanism whereby inhibition of Hsp90 disrupts free radical homeostasis and contributes directly to telomere erosion, further implicating Hsp90 as a potential therapeutic target for cancer cells.
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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.