ArticleBiochimica et biophysica acta2014
Lovastatin inhibits human B lymphoma cell proliferation by reducing intracellular ROS and TRPC6 expression.
Article in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- Crosstalk between calcium and reactive oxygen species signaling in cancer revisited.Cell calcium · 2025Review
- Article
- Investigating potential anti-proliferative activity of different statins against five cancer cell lines.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023Article
- Statins: a repurposed drug to fight cancer.Journal of experimental & clinical cancer research : CR · 2021Review
- Transient Receptor Potential (TRP) Channels in Haematological Malignancies: An Update.Biomolecules · 2021Review
- Cholesterol metabolism and tumor.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2021Review
- Cholesterol Stimulates the Transient Receptor Potential Melastatin 4 Channel in mpkCCDFrontiers in pharmacology · 2021Article
- NaHS or Lovastatin Attenuates Cyclosporine A-Induced Hypertension in Rats by Inhibiting Epithelial Sodium Channels.Frontiers in pharmacology · 2021Article
- Pleiotropic effects of statins: A focus on cancer.Biochimica et biophysica acta. Molecular basis of disease · 2020Review
- TRPC channels: Structure, function, regulation and recent advances in small molecular probes.Pharmacology & therapeutics · 2020Review
- Reactive Oxygen Species in Venous Thrombosis.International journal of molecular sciences · 2020Review
- The Two-Way Relationship Between Calcium and Metabolism in Cancer.Frontiers in cell and developmental biology · 2020Review
- Lovastatin attenuates hypertension induced by renal tubule-specific knockout of ATP-binding cassette transporter A1, by inhibiting epithelial sodium channels.British journal of pharmacology · 2019Article
- Cholesterol-enriched membrane microdomains are needed for insulin signaling and proliferation in hepatic cells.American journal of physiology. Gastrointestinal and liver physiology · 2018Article
- Monascus purpureus induced apoptosis on gastric cancer cell by scavenging mitochondrial reactive oxygen species.Journal of clinical biochemistry and nutrition · 2017Article
- Shielding of the geomagnetic field reduces hydrogen peroxide production in human neuroblastoma cell and inhibits the activity of CuZn superoxide dismutase.Protein & cell · 2017Article
- Crosstalk between calcium and reactive oxygen species signaling in cancer.Cell calcium · 2017Review
- Inhibition of TRPC6 reduces non-small cell lung cancer cell proliferation and invasion.Oncotarget · 2017Article
- Marketed drugs used for the management of hypercholesterolemia as anticancer armament.OncoTargets and therapy · 2017Review
- Chemomodulatory Potential of Bartogenic Acid Against DMBA/Croton Oil Induced Two-Step Skin Carcinogenesis in Mice.Journal of Cancer · 2016Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Clinical evidence suggests that statins reduce cancer incidence and mortality. However, there is lack of in vitro data to show the mechanism by which statins can reduce the malignancies of cancer cells. We used a human B lymphoma Daudi cells as a model and found that lovastatin inhibited, whereas exogenous cholesterol (Cho) stimulated, proliferation cell cycle progression in control Daudi cells, but not in the cells when transient receptor potential canonical 6 (TRPC6) channel was knocked down. Lovastatin decreased, whereas Cho increased, the levels of intracellular reactive oxygen species (ROS) respectively by decreasing or increasing the expression of p47-phox and gp91-phox (NOX2). Reducing intracellular ROS with either a mimetic superoxide dismutase (TEMPOL) or an NADPH oxidase inhibitor (apocynin) inhibited cell proliferation, particularly in Cho-treated cells. The effects of TEMPOL or apocynin were mimicked by inhibition of TRPC6 with SKF-96365. Lovastatin decreased TRPC6 expression and activity via a Cho-dependent mechanism, whereas Cho increased TRPC6 expression and activity via an ROS-dependent mechanism. Consistent with the fact that TRPC6 is a Ca(2+)-permeable channel, lovastatin decreased, but Cho increased, intracellular Ca(2+) also via ROS. These data suggest that lovastatin inhibits malignant B cell proliferation by reducing membrane Cho, intracellular ROS, TRPC6 expression and activity, and intracellular Ca(2+).
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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.