ArticleNaunyn-Schmiedeberg's archives of pharmacology2018
Suppression of glutathione S-transferases potentiates the cytotoxic effect of phenethyl isothiocyanate in cholangiocarcinoma cells.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Multiomics analysis of GSTP1 knockdown pancreatic cancer cells reveals key regulators of redox and metabolic homeostasis.Biology open · 2025Article
- Naturally Derived Phenethyl Isothiocyanate Modulates Induction of Oxidative Stress via ItsAntioxidants (Basel, Switzerland) · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phenethyl isothiocyanate (PEITC) is a potential cancer prevention agent that is found in cruciferous vegetables. Previous studies have shown that the effect of PEITC-induced cell death declines rapidly after administration. The metabolic fate of PEITC is modulated by glutathione S-transferases (GST). In this study, we investigated whether GST activity modulates PEITC-induced cytotoxicity on cholangiocarcinoma (CCA) cells. The sensitivity of KKU-M214 and KKU-100 cells to PEITC was associated with GST activity. Two GST inhibitors, ethacrynic acid (EA) and cibacron blue, potentiated the cytotoxic effect of PEITC in CCA cells. PEITC-induced glutathione (GSH) depletion and redox stress, whereas EA itself or in combination with PEITC did not alter GSH redox status. The enhanced cytotoxic effect of EA may be due to inhibition of GST activity. This idea was validated by using siRNA directed against GSTP1 mRNA in KKU-M214 cells, and GSTP1 and GSTT1 mRNA in KKU-100 cells. These GST isoforms were abundantly expressed in the cell lines. Knockdown of GSTs in CCA cell lines potentiated the cytotoxic effect of PEITC. The present study shows that the antitumor effect of PEITC was potentiated by the suppression of GST activity. The inhibition of GST could be a crucial strategy to potentiate chemotherapeutic effect of PEITC on CCA.
Indexed as
Identifiers
What 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.