ArticlePloS one2015
Paraptosis cell death induction by the thiamine analog benfotiamine in leukemia cells.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- A review on the role of cyclin dependent kinases in cancers.Cancer cell international · 2022Review
- Changes in Metabolic Profiles of Human Oral Cells by Benzylidene Ascorbates and Eugenol.Medicines (Basel, Switzerland) · 2018Article
- Effects of Combined Lysosomal and Mitochondrial Photodamage in a Non-small-Cell Lung Cancer Cell Line: The Role of Paraptosis.Photochemistry and photobiology · 2017Article
- Fusaric Acid immunotoxicity and MAPK activation in normal peripheral blood mononuclear cells and Thp-1 cells.Scientific reports · 2017Article
- Xanthohumol induces paraptosis of leukemia cells through p38 mitogen activated protein kinase signaling pathway.Oncotarget · 2017Article
- Non-Canonical Cell Death Induced by p53.International journal of molecular sciences · 2016Review
- Cytoplasmic vacuolization in cell death and survival.Oncotarget · 2016Review
- Effects of 3-styrylchromones on metabolic profiles and cell death in oral squamous cell carcinoma cells.Toxicology reports · 2015Article
- Article
- Biological Properties of the Aggregated Form of Chitosan Magnetic Nanoparticle.In vivo (Athens, Greece)Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Benfotiamine is a synthetic thiamine analogue that stimulates transketolase, a cellular enzyme essential for glucose metabolism. Currently, benfotiamine is used to treat diabetic neuropathy. We recently reported that oral benfotiamine induced a temporary but remarkable recovery from acute myeloid leukemia in an elderly patient who was ineligible for standard chemotherapy due to dementia and renal failure. In the present study we present evidences that benfotiamine possess antitumor activity against leukemia cells. In a panel of nine myeloid leukemia cell lines benfotiamine impaired the viability of HL-60, NB4, K562 and KG1 cells and also inhibited the growing of primary leukemic blasts. The antitumor activity of benfotiamine is not mediated by apoptosis, necrosis or autophagy, but rather occurs though paraptosis cell death induction. Mechanistic studies revealed that benfotiamine inhibited the activity of constitutively active ERK1/2 and concomitantly increased the phosphorylation of JNK1/2 kinase in leukemic cells. In addition, benfotiamine induced the down regulation of the cell cycle regulator CDK3 which resulted in G1 cell cycle arrest in the sensitive leukemic cells. Moreover, combination index studies showed that benfotiamine enhanced the antiproliferative activities of cytarabine against leukemia cells. These findings suggest that benfotiamine has antitumor therapeutic potential.
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