ArticleOncotarget2016
Cinobufagin inhibits tumor growth by inducing intrinsic apoptosis through AKT signaling pathway in human nonsmall cell lung cancer cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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.
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
28 citing papers in PubMed, 51 citations in OpenAlex.
- A narrative review of cinobufacini for endometrial cancer: mechanisms and therapeutic implications.Translational cancer research · 2026Review
- Cinobufagin Inhibits Invasion and Migration of Non-Small Cell Lung Cancer via Regulating Glucose Metabolism Reprogramming in Tumor-Associated Macrophages.Drug design, development and therapy · 2025Article
- Review
- Chemical Composition, Pharmacological Effects and Clinical Applications of Cinobufacini.Chinese journal of integrative medicine · 2024Review
- Cinobufagin disrupts the stability of lipid rafts by inhibiting the expression of caveolin-1 to promote non-small cell lung cancer cell apoptosis.Archives of medical science : AMS · 2024Article
- Article
- Article
- Cinobufagin exerts an antitumor effect in non-small-cell lung cancer by blocking STAT3 signaling.Journal of Cancer · 2023Article
- The mitochondrial protein YME1 Like 1 is important for non-small cell lung cancer cell growth.International journal of biological sciences · 2023Article
- The sodium/myo-inositol co-transporter SLC5A3 promotes non-small cell lung cancer cell growth.Cell death & disease · 2022Article
- Bersaldegenin-1,3,5-orthoacetate induces caspase-independent cell death, DNA damage and cell cycle arrest in human cervical cancer HeLa cells.Pharmaceutical biology · 2021Article
- Cinobufagin Exerts Anticancer Activity in Oral Squamous Cell Carcinoma Cells through Downregulation of ANO1.International journal of molecular sciences · 2021Article
- Drug-repurposing against COVID-19 by targeting a key signaling pathway: An in silico study.Medical hypotheses · 2021Article
- Cinobufagin-induced DNA damage response activates GCancer cell international · 2021Article
- Obacunone protects retinal pigment epithelium cells from ultra-violet radiation-induced oxidative injury.Aging · 2021Article
- Cinobufagin Is a Selective Anti-Cancer Agent against Tumors with EGFR Amplification and PTEN Deletion.Frontiers in pharmacology · 2021Article
- Cinobufagin Suppresses Melanoma Cell Growth by Inhibiting LEF1.International journal of molecular sciences · 2020Article
- The spinal microglial IL-10/β-endorphin pathway accounts for cinobufagin-induced mechanical antiallodynia in bone cancer pain following activation of α7-nicotinic acetylcholine receptors.Journal of neuroinflammation · 2020Article
- Cinobufagin inhibits tumor growth by inducing apoptosis through Notch signaling pathways in human cholangiocarcinoma.Translational cancer research · 2019Article
- Telocinobufagin and Marinobufagin Produce Different Effects in LLC-PK1 Cells: A Case of Functional Selectivity of Bufadienolides.International journal of molecular sciences · 2018Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
The cinobufagin (CB) has a broad spectrum of cytotoxicity to inhibit cell proliferation of various human cancer cell lines, but the molecular mechanisms still remain elusive. Here we observed that CB inhibited the cell proliferation and tumor growth, but induced cell cycle arrest and apoptosis in a dose-dependent manner in non-small cell lung cancer (NSCLC) cells. Treatment with CB significantly increased the reactive oxygen species but decreased the mitochondrial membrane potential in NSCLC cells. These effects were markedly blocked when the cells were pretreated with N-acetylcysteine, a specific reactive oxygen species inhibitor. Furthermore, treatment with CB induced the expression of BAX but reduced that of BCL-2, BCL-XL and MCL-1, leading to an activation of caspase-3, chromatin condensation and DNA degradation in order to induce programmed cell death in NSCLC cells. In addition, treatment with CB reduced the expressions of p-AKTT308 and p-AKTS473 and inhibited the AKT/mTOR signaling pathway in NSCLC cells in a time-dependent manner. Our results suggest that CB inhibits tumor growth by inducing intrinsic apoptosis through the AKT signaling pathway in NSCLC cells.
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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.