ArticlePloS one2014
Evodiamine induces G2/M arrest and apoptosis via mitochondrial and endoplasmic reticulum pathways in H446 and H1688 human small-cell lung cancer cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Antitumor Effects of Evodiamine in Mice Model Experiments: A Systematic Review and Meta-Analysis.Frontiers in oncology · 2021Pooled it
- Selective sensitivity of betel nut-related oral squamous cell carcinoma to evodiamine through cell cycle arrest, growth inhibition and apoptosis induction.Journal of Cancer · 2026Article
- Endoplasmic reticulum stress in non-small cell lung cancer: a review of therapeutic agents, mechanistic insights, and implications for therapy.Frontiers in cell and developmental biology · 2025Review
- Evodiamine: A Extremely Potential Drug Development Candidate of Alkaloids fromInternational journal of nanomedicine · 2024Review
- Evodiamine as an anticancer agent: a comprehensive review on its therapeutic application, pharmacokinetic, toxicity, and metabolism in various cancers.Cell biology and toxicology · 2023Review
- Roles of reactive oxygen species, mitochondrial membrane potential, and p53 in evodiamine-induced apoptosis and G2/M arrest of human anaplastic thyroid carcinoma cells.Chinese medicine · 2021Article
- Effect of superoxide dismutase, catalase, and glutathione reductase supplementation on cryopreservation of Black Bengal buck semen.Tropical animal health and production · 2021Article
- Research progress on evodiamine, a bioactive alkaloid ofExperimental and therapeutic medicine · 2021Review
- Curcumin Reverses NNMT-Induced 5-Fluorouracil Resistance via Increasing ROS and Cell Cycle Arrest in Colorectal Cancer Cells.Biomolecules · 2021Article
- Evodiamine in combination with histone deacetylase inhibitors has synergistic cytotoxicity in thyroid carcinoma cells.Endocrine · 2019Article
- Apoptotic Pathway as the Therapeutic Target for Anticancer Traditional Chinese Medicines.Frontiers in pharmacology · 2019Review
- Improved delivery of natural alkaloids into lung cancer through woody oil-based emulsive nanosystems.Drug delivery · 2018Article
- Evodiamine Induces Apoptosis in SMMC-7721 and HepG2 Cells by Suppressing NOD1 Signal Pathway.International journal of molecular sciences · 2018Article
- Antiproliferative Effects of Alkaloid Evodiamine and Its Derivatives.International journal of molecular sciences · 2018Review
- Homoisoflavanone-1 isolated fromOncology letters · 2018Article
- MicroRNA-137-regulated AKT serine/threonine kinase 2 inhibits tumor growth and sensitizes cisplatin in patients with non-small cell lung cancer.Oncology letters · 2018Article
- Sinularin Selectively Kills Breast Cancer Cells Showing G2/M Arrest, Apoptosis, and Oxidative DNA Damage.Molecules (Basel, Switzerland) · 2018Article
- Anticancer Activity of Natural and Synthetic Capsaicin Analogs.The Journal of pharmacology and experimental therapeutics · 2018Review
- Efficient intracellular delivery makes cancer cells sensitive to nanoemulsive chemodrugs.Oncotarget · 2017Article
- Evodiamine inhibits PDGF‑BB‑induced proliferation of rat vascular smooth muscle cells through the suppression of cell cycle progression and oxidative stress.Molecular medicine reports · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The goal of this study was to evaluate the ability of EVO to decrease cell viability and promote cell cycle arrest and apoptosis in small cell lung cancer (SCLC) cells. Lung cancer has the highest incidence and mortality rates among all cancers. Chemotherapy is the primary treatment for SCLC; however, the drugs that are currently used for SCLC are less effective than those used for non-small cell lung cancer (NSCLC). Therefore, it is necessary to develop new drugs to treat SCLC. In this study, the effects of evodiamine (EVO) on cell growth, cell cycle arrest and apoptosis were investigated in the human SCLC cell lines NCI-H446 and NCI-H1688. The results represent the first report that EVO can significantly inhibit the viability of both H446 and H1688 cells in dose- and time-dependent manners. EVO induced cell cycle arrest at G2/M phase, induced apoptosis by up-regulating the expression of caspase-12 and cytochrome C protein, and induced the expression of Bax mRNA and by down-regulating of the expression of Bcl-2 mRNA in both H446 and H1688 cells. However, there was no effect on the protein expression of caspase-8. Taken together, the inhibitory effects of EVO on the growth of H446 and H1688 cells might be attributable to G2/M arrest and subsequent apoptosis, through mitochondria-dependent and endoplasmic reticulum stress-induced pathways (intrinsic caspase-dependent pathways) but not through the death receptor-induced pathway (extrinsic caspase-dependent pathway). Our findings suggest that EVO is a promising novel and potent antitumor drug candidate for SCLC. Furthermore, the cell cycle, the mitochondria and the ER stress pathways are rational targets for the future development of an EVO delivery system to treat SCLC.
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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.