ArticleDiscover oncology2025
Gambogic acid suppresses osteosarcoma progression through upregulation of FOXO3a.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Hyaluronic Acid-Modified Redox-Responsive Gambogic Acid Prodrug Micelles for Targeted Therapy of Non-Small Cell Lung Cancer.International journal of nanomedicine · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
backgroundOsteosarcoma is a prevalent bone cancer in children and adolescents, posing significant treatment challenges due to its high metastatic potential and resistance to traditional chemotherapy. Gambogic Acid (GA), a natural compound, has demonstrated promising anticancer properties, including inhibition of cell proliferation and induction of apoptosis.
methodsThis study evaluated the anticancer effects of GA on osteosarcoma cell lines 143B and U2OS through cell viability assays, proliferation tests, wound healing assays, and flow cytometry to assess migration and apoptosis. RNA sequencing and RT-qPCR analyses were conducted to identify molecular mechanisms, with a focus on the tumor suppressor transcription factor FOXO3a. siRNA-mediated knockdown of FOXO3a was performed to determine its role in GA's mechanism of action.
resultsGA treatment significantly reduced cell viability and proliferation in a dose- and time-dependent manner, as shown by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and CCK-8 assays. Wound healing assays revealed a marked inhibition of cell migration, while flow cytometry confirmed a significant increase in apoptosis rates following GA treatment. RNA sequencing identified FOXO3a as a key upregulated gene in both cell lines after GA exposure, which was validated by RT-qPCR. Importantly, FOXO3a knockdown diminished GA's effects on cell viability, migration, and apoptosis, underscoring its pivotal role in mediating GA's anticancer activity.
conclusionsThe findings suggest that GA exerts potent anticancer effects on osteosarcoma cells through the upregulation of FOXO3a, a critical tumor suppressor. These results provide a foundation for further exploration of GA as a novel therapeutic agent for osteosarcoma, potentially offering a safer alternative to conventional chemotherapy. Future research will aim to elucidate the detailed mechanisms underlying the interaction between GA and FOXO3a and to optimize GA-based therapeutic strategies.
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.