ArticleOncology reports2016
Cinobufagin induces autophagy-mediated cell death in human osteosarcoma U2OS cells through the ROS/JNK/p38 signaling pathway.
Article in Oncology reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 28 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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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
28 citing papers in PubMed, 63 citations in OpenAlex.
- Natural products reshape osteosarcoma cell fate: promoting cell death.Frontiers in pharmacology · 2026Review
- Aniline TFPA enhances camptothecin-induced anti-NSCLC by modulating oxidative stress and impairing autophagy.Cancer cell international · 2025Article
- Cinobufagin treatments suppress tumor growth by enhancing the expression of cuproptosis-related genes in liver cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Molecular Mechanisms of the Therapeutic Effect of Selenium Nanoparticles in Hepatocellular Carcinoma.Cells · 2024Review
- Trends and future directions of autophagy in osteosarcoma: A bibliometric analysis.Open medicine (Warsaw, Poland) · 2024Review
- Pharmacological Effects of Cinobufagin.Medical science monitor : international medical journal of experimental and clinical research · 2023Article
- Amphibian-Derived Natural Anticancer Peptides and Proteins: Mechanism of Action, Application Strategies, and Prospects.International journal of molecular sciences · 2023Review
- Autophagy Modulation as a Potential Therapeutic Strategy in Osteosarcoma: Current Insights and Future Perspectives.International journal of molecular sciences · 2023Review
- Construction and validation of a prognostic model for osteosarcoma patients based on autophagy-related genes.Discover oncology · 2022Article
- Cinobufagin induces acute promyelocytic leukaemia cell apoptosis and PML-RARA degradation in a caspase-dependent manner by inhibiting the β-catenin signalling pathway.Pharmaceutical biology · 2022Article
- Screening of traditional Chinese medicine monomers as ribonucleotide reductase M2 inhibitors for tumor treatment.World journal of clinical cases · 2022Article
- Biologically synthesized black ginger-selenium nanoparticle induces apoptosis and autophagy of AGS gastric cancer cells by suppressing the PI3K/Akt/mTOR signaling pathway.Journal of nanobiotechnology · 2022Article
- Alisol B 23-Acetate Increases the Antitumor Effect of Bufalin on Liver Cancer through Inactivating Wnt/Computational and mathematical methods in medicine · 2022Article
- Network Pharmacology Prediction: The Possible Mechanisms of Cinobufotalin against Osteosarcoma.Computational and mathematical methods in medicine · 2022Article
- Natural compounds in the regulation of proteostatic pathways: An invincible artillery against stress, ageing, and diseases.Acta pharmaceutica Sinica. B · 2021Review
- Cinobufagin-induced DNA damage response activates GCancer cell international · 2021Article
- Triptolide inhibits JAK2/STAT3 signaling and induces lethal autophagy through ROS generation in cisplatin‑resistant SKOV3/DDP ovarian cancer cells.Oncology reports · 2021Article
- Establishment and verification of prognostic model for gastric cancer based on autophagy-related genes.American journal of cancer research · 2021Article
- Cinobufagin Suppresses Melanoma Cell Growth by Inhibiting LEF1.International journal of molecular sciences · 2020Article
- Costunolide Induces Autophagy and Apoptosis by Activating ROS/MAPK Signaling Pathways in Renal Cell Carcinoma.Frontiers in oncology · 2020Article
Corrections and comments
- Retraction · 2025-06-16Concerns/Issues about Data · Duplication of Data · Error in Image · Euphemisms for Duplication · Euphemisms for Plagiarism · Investigation by Journal/Publisher · Investigation by Third Party · Plagiarism of Data · · See also: https://pubpeer.com/publications/9EDCF4E6CDC50FF4A70A43EFD7F51E
- Retracted
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The main objective of this study was to explore whether autophagy could be triggered by cinobufagin, and to clarify the role of autophagy in the antitumor effects of cinobufagin on U2OS cells and the underlying mechanisms. U2OS cells were exposed to 15, 30, 60 and 120 mg/l cinobufagin for 0, 12, 24 and 48 h. An MTT assay was used to measure cell viability. FITC-Annexin Ⅴ/PI staining and flow cytometry were used to analyze the apoptotic ratio, while apoptotic morphological changes were assessed by PI and Hoechst 33258 viable cell staining. The effects of autophagy on the cells were investigated with GFP-LC3b green fluorescence plasmid transfection and transmission electron microscopy. The levels of caspase-3, -8, - 9, cleaved PARP, LC3-II/LC3-I, p62 and the activation of JNK/p-38 were detected by western blot analysis. Reactive oxygen species (ROS) fluorescence intensity was examined under fluorescence microscopy with an analysis software system. Cell proliferation was obviously inhibited by cinobufagin in a dose- and time-dependent manner. The apoptosis ratio was gradually increased with treatment time as evidenced by flow cytometric analysis and Hoechst 33258 staining. Exposure to cinobufagin resulted in the activation of caspase-3, -8, -9, as well as cleaved PARP which indicated that cinobufagin induced caspase-dependent apoptosis. Autophagy was confirmed in the cinobufagin-treated cells as evidenced by formation of autophagosomes, accumulation of GFP-LC3 fluorescence particles as well as the upregulation of LC3-II/LC3-I levels. Inhibition of autophagy diminished apoptosis as detected by the MTT assays. Moreover the percentage of apoptotic cells decreased following pretreatment with 3-MA, CQ and si-beclin-1. Cinobufagin also induced phosphorylation of the JNK and p38 signaling pathway as well as ROS generation. The JNK and p38 inhibitors significantly attenuated coexistence of apoptosis and autophagy-related proteins. The ROS scavenger also prevented phosphorylation of the JNK and p38 signaling pathway. Our research proved that cinobufagin triggered apoptosis and autophagic cell death via activation of the ROS/JNK/p-38 axis.
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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.