ArticlePloS one2013
Golden berry-derived 4β-hydroxywithanolide E for selectively killing oral cancer cells by generating ROS, DNA damage, and apoptotic pathways.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 97 citations in OpenAlex.
- Management of triple-negative breast cancer by natural compounds through different mechanistic pathways.Frontiers in genetics · 2024Review
- The Protective Role of Cranberries and Blueberries in Oral Cancer.Plants (Basel, Switzerland) · 2023Review
- Hairy root culture: a potent method for improved secondary metabolite production of Solanaceous plants.Frontiers in plant science · 2023Review
- Antiproliferation Effects of Marine-Sponge-Derived Methanol Extract ofAntioxidants (Basel, Switzerland) · 2022Article
- Methanol Extract ofAntioxidants (Basel, Switzerland) · 2022Article
- Physapruin A Enhances DNA Damage and Inhibits DNA Repair to Suppress Oral Cancer Cell Proliferation.International journal of molecular sciences · 2022Article
- Impacts of Oxidative Stress and PI3K/AKT/mTOR on Metabolism and the Future Direction of Investigating Fucoidan-Modulated Metabolism.Antioxidants (Basel, Switzerland) · 2022Review
- Identification of autophagy-related biomarker and analysis of immune infiltrates in oral carcinoma.Journal of clinical laboratory analysis · 2022Article
- Brown Algae-Derived Fucoidan Exerts Oxidative Stress-Dependent Antiproliferation on Oral Cancer Cells.Antioxidants (Basel, Switzerland) · 2022Article
- Combined Treatment with Cryptocaryone and Ultraviolet C Promotes Antiproliferation and Apoptosis of Oral Cancer Cells.International journal of molecular sciences · 2022Article
- Antiproliferation- and Apoptosis-Inducible Effects of a Novel Nitrated [6,6,6]Tricycle Derivative (SK2) on Oral Cancer Cells.Molecules (Basel, Switzerland) · 2022Article
- Burmannic Acid Inhibits Proliferation and Induces Oxidative Stress Response of Oral Cancer Cells.Antioxidants (Basel, Switzerland) · 2021Article
- Lactucin induces apoptosis through reactive oxygen species-mediated BCL-2 and CFLARGenes & genomics · 2021Article
- Stimulation of ROS Generation by Extract ofAntioxidants (Basel, Switzerland) · 2021Article
- Article
- Article
- Pomegranate Extract (POMx) Induces Mitochondrial Dysfunction and Apoptosis of Oral Cancer Cells.Antioxidants (Basel, Switzerland) · 2021Article
- Withaferin A Triggers Apoptosis and DNA Damage in Bladder Cancer J82 Cells through Oxidative Stress.Antioxidants (Basel, Switzerland) · 2021Article
- Article
- Combined Treatment with Low Cytotoxic Ethyl AcetateAntioxidants (Basel, Switzerland) · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMost chemotherapeutic drugs for killing cancer cells are highly cytotoxic in normal cells, which limits their clinical applications. Therefore, a continuing challenge is identifying a drug that is hypersensitive to cancer cells but has minimal deleterious effects on healthy cells. The aims of this study were to evaluate the potential of 4β-hydroxywithanolide (4βHWE) for selectively killing cancer cells and to elucidate its related mechanisms. METHODOLOGY AND PRINCIPAL
findingsChanges in survival, oxidative stress, DNA damage, and apoptosis signaling were compared between 4βHWE-treated oral cancer (Ca9-22) and normal fibroblast (HGF-1) cells. At 24 h and 48 h, the numbers of Ca9-22 cells were substantially decreased, but the numbers of HGF-1 cells were only slightly decreased. Additionally, the IC50 values for 4βHWE in the Ca9-22 cells were 3.6 and 1.9 µg/ml at 24 and 48 h, respectively. Time-dependent abnormal increases in ROS and dose-responsive mitochondrial depolarization can be exploited by using 4βHWE in chemotherapies for selectively killing cancer cells. Dose-dependent DNA damage measured by comet-nuclear extract assay and flow cytometry-based γ-H2AX/propidium iodide (PI) analysis showed relatively severer damage in the Ca9-22 cells. At both low and high concentrations, 4βHWE preferably perturbed the cell cycle in Ca9-22 cells by increasing the subG1 population and arrest of G1 or G2/M. Selective induction of apoptosis in Ca9-22 cells was further confirmed by Annexin V/PI assay, by preferential expression of phosphorylated ataxia-telangiectasia- and Rad3-related protein (p-ATR), and by cleavage of caspase 9, caspase 3, and poly ADP-ribose polymerase (PARP). CONCLUSIONS/SIGNIFICANCE: Together, the findings of this study, particularly the improved understanding of the selective killing mechanisms of 4βHWE, can be used to improve efficiency in killing oral cancer cells during chemoprevention and therapy.
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.