ArticleThe Journal of pharmacology and experimental therapeutics2011
Aborted autophagy and nonapoptotic death induced by farnesyl transferase inhibitor and lovastatin.
Article in The Journal of pharmacology and experimental therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Genetic and pharmacological modulation of lamin A farnesylation determines its function and turnover.Aging cell · 2024Article
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- Repurposing Drugs in Small Animal Oncology.Animals : an open access journal from MDPI · 2022Review
- Novel Effects of Statins on Cancer via Autophagy.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Statins: a repurposed drug to fight cancer.Journal of experimental & clinical cancer research : CR · 2021Review
- Targeting the Tumor Microenvironment: A Literature Review of the Novel Anti-Tumor Mechanism of Statins.Frontiers in oncology · 2021Review
- Implications on the Therapeutic Potential of StatinsOxidative medicine and cellular longevity · 2021Review
- A farnesyltransferase inhibitor activates lysosomes and reduces tau pathology in mice with tauopathy.Science translational medicine · 2019Article
- Ras and Rap1: A tale of two GTPases.Seminars in cancer biology · 2019Review
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- The Interplay Between Apolipoprotein E4 and the Autophagic-Endocytic-Lysosomal Axis.Molecular neurobiology · 2018Review
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- Caveolae as a target to quench autoinduction of the metastatic phenotype in lung cancer.Journal of cancer research and clinical oncology · 2016Article
- How to Target Activated Ras Proteins: Direct Inhibition vs. Induced Mislocalization.Mini reviews in medicinal chemistry · 2016Review
- Spatial Metrics of Tumour Vascular Organisation Predict Radiation Efficacy in a Computational Model.PLoS computational biology · 2016Article
- Mechanisms for autophagy modulation by isoprenoid biosynthetic pathway inhibitors in multiple myeloma cells.Oncotarget · 2015Article
- A combination therapy for KRAS-driven lung adenocarcinomas using lipophilic bisphosphonates and rapamycin.Science translational medicine · 2014Article
- Ras and autophagy in cancer development and therapy.Oncotarget · 2014Review
- Activated Ras as a Therapeutic Target: Constraints on Directly Targeting Ras Isoforms and Wild-Type versus Mutated Proteins.ISRN oncology · 2013Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Exposure of the human malignant peripheral nerve sheath tumor cell lines STS-26T, ST88-14, and NF90-8 to nanomolar concentrations of both lovastatin and farnesyl transferase inhibitor (FTI)-1 but not to either drug alone induced cell death. ST88-14 and NF90-8 cells underwent apoptosis, yet dying STS-26T cells did not. FTI-1 cotreatment induced a strong and sustained autophagic response as indicated by analyses of microtubule-associated protein-1 light chain 3 (LC3)-II accumulation in STS-26T cultures. Extensive colocalization of LC3-positive punctate spots was observed with both lysosome-associated membrane protein (LAMP)-1 and LAMP-2 (markers of late endosomes/lysosomes) in solvent or FTI-1 or lovastatin-treated STS-26T cultures but very little colocalization in lovastatin/FTI-1-cotreated cultures. The absence of colocalization in the cotreatment protocol correlated with loss of LAMP-2 expression. Autophagic flux studies indicated that lovastatin/FTI-1 cotreatment inhibited the completion of the autophagic program. In contrast, rapamycin induced an autophagic response that was associated with cytostasis but maintenance of viability. These studies indicate that cotreatment of STS-26T cells with lovastatin and FTI-1 induces an abortive autophagic program and nonapoptotic cell death.
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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.