ArticleOncology letters2019
Propyl isothiocyanate induces apoptosis in gastric cancer cells by oxidative stress via glutathione depletion.
Article in Oncology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 7 citations in OpenAlex.
- New Functions of Mitochondrial Dysfunction in Gastric Cancer: From Molecular Processes to Potential Treatments.International journal of molecular sciences · 2026Review
- Quantitative chemical proteomics reveals that phenethyl isothiocyanate covalently targets BID to promote apoptosis.Cell death discovery · 2024Article
- Assessment of Methodological Pipelines for the Determination of Isothiocyanates Derived from Natural Sources.Antioxidants (Basel, Switzerland) · 2022Review
- Characterisation of naturally occurring isothiocyanates as glutathione reductase inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2020Article
- Knockdown of SLC35F2 Inhibits the Proliferation and Metastasis of Bladder Cancer Cells.OncoTargets and therapy · 2019Article
Corrections and comments
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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
Isothiocyanates are a group of compounds that exist in the majority of cruciferous plants. A number of isothiocyanates have been demonstrated to exhibit anticancer effects; however, antitumor properties of propyl isothiocyanate (PITC) have not been evaluated previously. In this study, the possible effects of PITC on gastric cancer (GC) cells were investigated, and the potential underlying mechanisms were explored. The results demonstrated that PITC inhibited cell viability of two GC cell lines and induced cell cycle arrest and apoptosis. Treatment with PITC promoted total glutathione depletion in GC cell lines, leading to reactive oxygen species accumulation and DNA damage, which activated the mitochondria-dependent and p53 signaling pathways to trigger apoptosis in GC cells. The effects of PITC were reversed by N-Acetyl-L-cysteine. The results of the present study revealed the potential mechanisms of PITC on apoptosis induction in GC cells, which may be mediated by mitochondria-dependent apoptosis and DNA damage.
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Registered trials
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