ArticleBritish journal of pharmacology2006
Lovastatin protects human endothelial cells from the genotoxic and cytotoxic effects of the anticancer drugs doxorubicin and etoposide.
Article in British journal of pharmacology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 82 citations in OpenAlex.
- Mitigation of Radiation-induced Acute Hematopoietic System and Intestine Injury by Resveratrol-loaded Polymeric Nanoparticles after Whole Body Irradiation in Mice.Current radiopharmaceuticals · 2025Article
- An integrative review of nonobvious puzzles of cellular and molecular cardiooncology.Cellular & molecular biology letters · 2023Review
- Atorvastatin Can Modulate DNA Damage Repair in Endothelial Cells Exposed to Mitomycin C.International journal of molecular sciences · 2023Article
- Molecular mechanisms of anthracycline cardiovascular toxicity.Clinical science (London, England : 1979) · 2021Review
- Article
- Effects of melatonin on the Bisphenol-A- induced cytotoxicity and genetic toxicity in colon cancer cell lines, normal gingival cell lines, and bone marrow stem cell lines.Cancer informatics · 2021Article
- MicroRNAs in Cancer Treatment-Induced Cardiotoxicity.Cancers · 2020Review
- Atorvastatin DownregulatesOxidative medicine and cellular longevity · 2018Article
- Doxorubicin upregulates CXCR4 via miR-200c/ZEB1-dependent mechanism in human cardiac mesenchymal progenitor cells.Cell death & disease · 2017Article
- Rho inhibition by lovastatin affects apoptosis and DSB repair of primary human lung cells in vitro and lung tissue in vivo following fractionated irradiation.Cell death & disease · 2017Article
- Statins in anthracycline-induced cardiotoxicity: Rac and Rho, and the heartbreakers.Cell death & disease · 2017Review
- Lovastatin prevents bleomycin-induced DNA damage to HepG2 cells.Research in pharmaceutical sciences · 2016Article
- Targeting endothelial cell metabolism for cardio-protection from the toxicity of antitumor agents.Cardio-oncology (London, England) · 2016Review
- Rho GTPases: Novel Players in the Regulation of the DNA Damage Response?Biomolecules · 2015Review
- Cardiac risk in the treatment of breast cancer: assessment and management.Breast cancer (Dove Medical Press) · 2015Review
- Cancer therapy-induced cardiotoxicity: basic mechanisms and potential cardioprotective therapies.Journal of the American Heart Association · 2014Review
- Chemotherapy-Induced Cardiotoxicity: Pathophysiology and Prevention.Clujul medical (1957) · 2014Review
- Protective role of atorvastatin against doxorubicin-induced cardiotoxicity and testicular toxicity in mice.Journal of physiology and biochemistry · 2013Article
- Rac1 modulates acute and subacute genotoxin-induced hepatic stress responses, fibrosis and liver aging.Cell death & disease · 2013Article
- Rac1 protein signaling is required for DNA damage response stimulated by topoisomerase II poisons.The Journal of biological chemistry · 2012Article
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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
background and purpose3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) are frequently used lipid-lowering drugs. Moreover, they exert pleiotropic effects on cellular stress responses and death. Here, we analysed whether lovastatin affects the sensitivity of primary human endothelial cells (HUVEC) to the anticancer drug doxorubicin. EXPERIMENTAL APPROACH: We investigated whether pretreatment of HUVEC with low dose of lovastatin influences the cellular sensitivity to doxorubicin. To this end, cell viability, proliferation and apoptosis as well as DNA damage-triggered stress response were analysed. KEY
resultsLovastatin reduced the cytotoxic potency of doxorubicin in HUVEC. Lovastatin attenuated the doxorubicin-induced increase in p53 as well as activation of checkpoint kinase (Chk-1) and stress-activated protein kinase/c-Jun-N-terminal kinase (SAPK/JNK). Acquired doxorubicin resistance was independent of alterations in doxorubicin efflux and cell cycle progression. Also, doxorubicin-triggered production of reactive oxygen species (ROS) and formation of oxidative DNA lesions remained unaffected by lovastatin. However, lovastatin impaired DNA strand break formation induced by doxorubicin. Notably, lovastatin also conferred cross-resistance to the cytotoxic and genotoxic effects of etoposide, indicating that lovastatin shields topoisomerase II against poisons. CONCLUSIONS AND IMPLICATIONS: Based on these data, we suggest that lovastatin-mediated resistance to topoisomerase II inhibitors is due to a reduction in DNA damage and, hence, it attenuates stress responses leading to cell death that are triggered by DNA damage. Therefore, lovastatin might be useful clinically for alleviating side-effects of anticancer therapies that include topoisomerase II inhibitors.
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