ArticleRedox biology2017
Induction of reactive oxygen species-stimulated distinctive autophagy by chelerythrine in non-small cell lung cancer cells.
Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 70 citations in OpenAlex.
- Sanguinarine Antagonizes NSCLC Through PPARG-Mediated PI3K/AKT Suppression and Autophagic Apoptosis.Cell biochemistry and biophysics · 2026Article
- Chelerythrine Inhibits TGF-β-Induced Epithelial-Mesenchymal Transition in A549 Cells via RRM2.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Unlocking the dual role of autophagy: A new strategy for treating lung cancer.Journal of pharmaceutical analysis · 2025Review
- Traditional Chinese medicine in lung cancer treatment.Molecular cancer · 2025Review
- Combining network pharmacology and molecular docking to explore the pharmacological mechanism of Codonopsis Radix.-Hedysarum Multijugum Maxim.-Atractylodes Macrocephala Koidz. in treating lung cancer.BMC complementary medicine and therapies · 2025Article
- The Phytochemical Profile of the Petroleum Ether Extract ofInternational journal of molecular sciences · 2024Article
- Molecular probes for tracking lipid droplet membrane dynamics.Nature communications · 2024Article
- Recent Advances in Alkaloids fromMolecules (Basel, Switzerland) · 2024Review
- Comprehensiveness cuproptosis related genes study for prognosis and medication sensitiveness across cancers, and validation in prostate cancer.Scientific reports · 2024Article
- Osimertinib induces paraptosis and TRIP13 confers resistance in glioblastoma cells.Cell death discovery · 2023Article
- DNA repair pathways-targeted cyclovirobuxine inhibits castration-resistant prostate cancer growth by promoting cell apoptosis and cycle arrest.Translational oncology · 2023Article
- Article
- Natural compounds targeting mitochondrial dysfunction: emerging therapeutics for target organ damage in hypertension.Frontiers in pharmacology · 2023Review
- Chelerythrine-Induced Apoptotic Cell Death in HepG2 Cells Involves the Inhibition of Akt Pathway and the Activation of Oxidative Stress and Mitochondrial Apoptotic Pathway.Antioxidants (Basel, Switzerland) · 2022Article
- Fluorescence, Absorption, Chromatography and Structural Transformation of Chelerythrine and Ethoxychelerythrine in Protic Solvents: A Comparative Study.Molecules (Basel, Switzerland) · 2022Article
- Review
- Chelerythrine Chloride Inhibits Stemness of Melanoma Cancer Stem-Like Cells (CSCs) Potentially via Inducing Reactive Oxygen Species and Causing Mitochondria Dysfunction.Computational and mathematical methods in medicine · 2022Article
- Rediscovery of Traditional Plant Medicine: An Underestimated Anticancer Drug of Chelerythrine.Frontiers in pharmacology · 2022Review
- The Anticancer Effect of Natural Plant Alkaloid Isoquinolines.International journal of molecular sciences · 2021Review
- Suppression of LETM1 inhibits the proliferation and stemness of colorectal cancer cells through reactive oxygen species-induced autophagy.Journal of cellular and molecular medicine · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chelerythrine (CHE), a natural benzo[c]phenanthridine alkaloid, shows anti-cancer effect through a number of mechanisms. Herein, the effect and mechanism of the CHE-induced autophagy, a type II programmed cell death, in non-small cell lung cancer (NSCLC) cells were studied for the first time. CHE induced cell viability decrease, colony formation inhibition, and apoptosis in a concentration-dependent manner in NSCLC A549 and NCI-H1299 cells. In addition, CHE triggered the expression of phosphatidylethanolamine-modified microtubule-associated protein light-chain 3 (LC3-II). The CHE-induced expression of LC3-II was further increased in the combination treatment with chloroquine (CQ), an autophagy inhibitor, and large amounts of red-puncta were observed in the CHE-treated A549 cells with stable expression of mRFP-EGFP-LC3, indicating that CHE induces autophagy flux. Silence of beclin 1 reversed the CHE-induced expression of LC3-II. Inhibition of autophagy remarkably reversed the CHE-induced cell viability decrease and apoptosis in NCI-H1299 cells but not in A549 cells. Furthermore, CHE triggered reactive oxygen species (ROS) generation in both cell lines. A decreased level of ROS through pretreatment with N-acetyl-L-cysteine reversed the CHE-induced cell viability decrease, apoptosis, and autophagy. Taken together, CHE induced distinctive autophagy in A549 (accompanied autophagy) and NCI-H1299 (pro-death autophagy) cells and a decreased level of ROS reversed the effect of CHE in NSCLC cells in terms of cell viability, apoptosis, and autophagy.
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Registered trials
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