ArticleOncology letters2018
Dihydromyricetin induces apoptosis in a human choriocarcinoma cell line.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Multiple molecular and cellular mechanisms of the antitumour effect of dihydromyricetin (Review).Biomedical reports · 2024Review
- Present Status, Challenges, and Prospects of Dihydromyricetin in the Battle against Cancer.Cancers · 2022Review
- Advanced maternal age causes premature placental senescence and malformation via dysregulated α-Klotho expression in trophoblasts.Aging cell · 2021Article
- Dihydromyricetin Acts as a Potential Redox Balance Mediator in Cancer Chemoprevention.Mediators of inflammation · 2021Review
- Inhibitory effect of dihydromyricetin on the proliferation of JAR cells and its mechanism of action.Oncology letters · 2020Article
- Dihydromyricetin Attenuates Metabolic Syndrome And Improves Insulin Sensitivity By Upregulating Insulin Receptor Substrate-1 (Y612) Tyrosine Phosphorylation In db/db Mice.Diabetes, metabolic syndrome and obesity : targets and therapy · 2019Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Choriocarcinoma is a malignant trophoblastic tumor. The development of novel drugs is required to reduce the toxicity of current multi-agent chemotherapy and to successfully treat chemoresistant cases of the disease. The purpose of the present study was to investigate the effect of dihydromyricetin (DMY) on the human choriocarcinoma cell line, JAr, to identify a novel drug for the treatment of choriocarcinoma. An MTT assay was performed to determine the effects of DMY at different concentrations and for different exposure durations. Flow cytometry and TUNEL assays were performed to detect apoptosis, and western blotting was utilized to investigate the underlying mechanism. The results revealed that DMY significantly inhibited JAr cell viability in a time- and dose-dependent manner. The flow cytometry and TUNEL assays demonstrated that DMY inhibited proliferation by inducing apoptosis. Further analysis by western blotting indicated that the protein expression level of BCL-2 associated X, associated protein increased, while the protein expression levels of BCL-2 and pro-caspase-3 decreased. These findings suggest that DMY induced apoptosis in human choriocarcinoma JAr cells, through a mitochondrially mediated apoptotic pathway.
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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.