ArticleInternational journal of clinical and experimental pathology2017
Lovastatin induces apoptosis of HepG-2 cells by activating ROS-dependent mitochondrial and ER stress pathways.
Article in International journal of clinical and experimental pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 6 citations in OpenAlex.
- Statins as Potential Preventative Treatment of ETX and Multiple Pore-Forming Toxin-Induced Diseases.International journal of molecular sciences · 2023Article
- Familial hypercholesterolemia class II low-density lipoprotein receptor response to statin treatment.Disease models & mechanisms · 2020Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
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Abstract
backgroundStatins can reduce the malignancies through stimulating apoptosis. We aimed to elucidate the role of lovastatin in HepG-2 cells.
methodsHepG-2 and non-tumor L-O2 cells were used as the cell models. CCK-8, flow cytometric analysis and carboxy fluorescein diacetate succinimidyl ester (CFDA-SE) labeling were performed to monitor the viability, apoptosis and proliferation.
resultsWe found that lovastatin exerted the most tumor suppressing effects on liver cancer cells among the three tested statins. Lovastatin treatment significantly reduced cell viability and proliferation, and induced apoptosis in HepG-2. However, drug resistance effects were observed in the non-tumor L-O2 cells. The apoptosis triggered by lovastatin was accompanied by high intracellular levels of ROS. Pretreatment with the ROS blocker N-acetyl-cysteine (NAC) could mitigate the lovastatin-induced cytotoxicity in HepG-2 cells. Mechanistically, lovastatin increased HepG-2 cell apoptosis by triggering mitochondrial and endoplasmic reticulum (ER) stress pathways through ROS accumulation.
conclusionsLovastatin significantly induced cell apoptosis by activating ROS-dependent mitochondrial and ER stress pathways in HepG-2 cells.
Indexed as
Identifiers
31966503PMC6966085W3015535205What OpenQuestion holds
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.