ArticleMolecular medicine reports2016
Arsenic trioxide and triptolide synergistically induce apoptosis in the SKM‑1 human myelodysplastic syndrome cell line.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 11 citations in OpenAlex.
- Article
- Single-cell transcriptome sequencing reveals the mechanism of Realgar improvement on erythropoiesis in mice with myelodysplastic syndrome.Cancer cell international · 2025Article
- Role of reactive oxygen species in myelodysplastic syndromes.Cellular & molecular biology letters · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although certain combination therapies comprising arsenic trioxide (As2O3) with other agents exist for the treatment of several types of human cancer, few As2O3 combination therapies are clinically effective for myelodysplastic syndromes (MDS). Triptolide (TL) may be an effective therapeutic agent for the treatment of MDS. However, to date, there is no combination therapy for MDS with As2O3 and TL. Therefore, the aim of the present study was to investigate this combination therapy on the apoptosis of MDS SKM‑1 cells. The MDS SKM‑1 cells were treated with As2O3, TL or the two in combination at various concentrations, or were mock‑treated. Cell viability, cell apoptosis, levels of reactive oxygen species (ROS) and the expression of the cell apoptosis‑associated genes, B cell lymphoma‑2 (Bcl‑2), Bcl‑2‑associated X protein (Bax) and caspase‑3, were determined using an MTT assay, flow cytometric analysis of annexin V‑fluorescein isothiocyanate/propidium iodide double‑stained cells, flow cytometic analysis of intracellular 2',7'‑dichlorodihydrofluorescein diacetate fluorescence and reverse transcription‑quantitative polymerase chain reaction analysis, respectively. Combination index (CI) analysis was performed to determine whether effects were synergistic (CI<1). The combination treatment was found to synergistically inhibit MDS SKM‑1 cell growth, induce cell apoptosis, increase ROS levels, upregulate the expression levels of Bax and caspase‑3, and downregulate the mRNA expression of Bcl‑2. In conclusion, the combination treatment of As2O3 and TL synergistically induced apoptosis in the MDS SKM‑1 cells.
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.