ArticleBMC complementary and alternative medicine2019
Calotropis gigantea extract induces apoptosis through extrinsic/intrinsic pathways and reactive oxygen species generation in A549 and NCI-H1299 non-small cell lung cancer cells.
Article in BMC complementary and alternative medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- From traditional uses to biochemical evidence: phytochemical diversity and bioactivities of Calotropis gigantea-a comprehensive update since 2013.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026Review
- Cytotoxicity evaluation of3 Biotech · 2025Article
- MAT1A activation of glycolysis to promote NSCLC progression depends on stabilizing CCND1.Cell death & disease · 2024Article
- Combination of ethyl acetate fraction from Calotropis gigantea stem bark and sorafenib induces apoptosis in HepG2 cells.PloS one · 2024Article
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- Antitumor effect and molecular mechanism of fucoidan in NSCLC.BMC complementary medicine and therapies · 2021Article
- Calotropis gigantea stem bark extract induced apoptosis related to ROS and ATP production in colon cancer cells.PloS one · 2021Article
- Pharmaceutical characterization and exploration of Arkeshwara rasa in MDA-MB-231 cells.Journal of Ayurveda and integrative medicineArticle
- Circ_0003998 Regulates the Progression and Docetaxel Sensitivity of DTX-Resistant Non-Small Cell Lung Cancer Cells by the miR-136-5p/CORO1C Axis.Technology in cancer research & treatmentArticle
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11 authors.
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Abstract
backgroundCalotropis gigantea (CG) is a tall and waxy flower that is used as a traditional remedy for fever, indigestion, rheumatism, leprosy, and leukoderma. However, the precise mechanisms of its anticancer effects have not yet been examined in human non-small cell lung cancer (NSCLC) cells. In this study, we investigated whether CG extract exerted an apoptotic effect in A549 and NCI-H1299 NSCLC cells.
methodsThe ethanol extract of CG was prepared, and its apoptotic effects on A549 and NCI-H1299 NSCLC cells were assessed by using the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxy methoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay, annexin V-fluorescein isothiocyanate/propidium iodide (PI) staining, cell cycle analysis, real-time polymerase chain reaction (RT-PCR), western blotting, JC-1 staining, and ROS detection assay.
resultsThe CG extract induced apoptosis through the stimulation of intrinsic and extrinsic signaling pathways in A549 and NCI-H1299 lung cancer cells. Cell cycle arrest was induced by the CG extract in both cell lines. Reactive oxygen species (ROS), which can induce cell death, were also generated in the CG-treated A549 and NCI-H1299 cells.
conclusionsThese data confirmed that CG caused apoptosis through the activation of extrinsic and intrinsic pathways, cell cycle arrest, and ROS generation in A549 and NCI-H1299 lung cancer cells. Thus, CG can be suggested as a potential agent for lung cancer therapy.
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