ArticleOncology letters2019
Arsenic compounds induce apoptosis through caspase pathway activation in MA-10 Leydig tumor cells.
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 7 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
7 citing papers in PubMed, 14 citations in OpenAlex.
- Heavy Metal-Contaminated Soils and Gastric Cancer Risk: Molecular Insights and the Relevance of a One Health Perspective.International journal of molecular sciences · 2025Review
- CRISPR/Cas9-Based Modeling ofInternational journal of molecular sciences · 2025Article
- Can quercetin reduce arsenic induced toxicity in mouse BALB/c 3T3 fibroblast cells? A study involving in vitro, molecular docking, and ADME predictions.BMC pharmacology & toxicology · 2025Article
- Arsenic and Benzo[a]pyrene Co-exposure Effects on MDA-MB-231 Cell Viability and Migration.Biological trace element research · 2025Article
- Sodium arsenite and dimethylarsenic acid induces apoptosis in OC3 oral cavity cancer cells.Molecular medicine reports · 2023Article
- Mitochondrial ROS, ER Stress, and Nrf2 Crosstalk in the Regulation of Mitochondrial Apoptosis Induced by Arsenite.Antioxidants (Basel, Switzerland) · 2022Review
- Targeting Cell Death Mechanism Specifically in Triple Negative Breast Cancer Cell Lines.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The incidence of testicular cancer is increasing worldwide. Leydig cell tumors represent one type of sex cord-stromal testis malignancy, which tend to respond unfavorably to chemotherapies. Identifying more efficient treatment strategies is therefore crucial for patients. The present study aimed to investigate the apoptotic effects of arsenic compounds and their underlying mechanisms. The results indicated that sodium arsenite and dimethylarsenic acid induced apoptosis of the murine Leydig tumor cell line, MA-10. These apoptotic effects were characterized morphologically by membrane blebbing and cell detachment assays, biochemically using a cell viability assay, and cytologically by flow cytometry analysis. Western blotting demonstrated that caspases-3, -8 and -9, and poly(ADP-ribose) polymerase protein levels were increased compared with untreated MA-10 cells; however, the caspase inhibitor, Z-VAD-fmk, reversed these effects. In conclusion, the present study has shown that sodium arsenite and dimethylarsenic acid may activate the intrinsic and extrinsic caspase pathways, and induce MA-10 cell apoptosis. These results suggest that sodium arsenite and dimethylarsenic acid may represent novel approaches to treat clinically unmanageable forms of testicular cancer.
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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.