ArticleIranian journal of medical sciences2019
The Calotropis Gigantea Methanolic Extract Induces Apoptosis in Human Breast Carcinoma Cells.
Article in Iranian journal of medical sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Machine learning for discovering anticancer compounds from plants and elucidating their mechanisms.Journal of computer-aided molecular design · 2026Review
- Unveiling the therapeutic potential of Calotropis procera: from traditional applications to phytochemistry, pharmacology, and safety.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026Review
- 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
- HPLC-MS standardization and validation methods for determination of calactin content in dichloromethane fraction ofHeliyon · 2025Article
- Combination of ethyl acetate fraction from Calotropis gigantea stem bark and sorafenib induces apoptosis in HepG2 cells.PloS one · 2024Article
- Comparative study of microscale and macroscale technique for encapsulation of Calotropis gigantea extract in metal-conjugated nanomatrices for invasive ductal carcinoma.Scientific reports · 2023Article
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- An updated pharmacological insight into calotropin as a potential therapeutic agent in cancer.Frontiers in pharmacology · 2023Review
- Calotropis gigantea stem bark extracts inhibit liver cancer induced by diethylnitrosamine.Scientific reports · 2022Article
- Calotropis gigantea stem bark extract induced apoptosis related to ROS and ATP production in colon cancer cells.PloS one · 2021Article
- Unveiling the anti-cancer mechanisms of calotropin: Insights into cell growth inhibition, cell cycle arrest, and metabolic regulation in human oral squamous carcinoma cells (HSC-3).Journal of oral biology and craniofacial researchArticle
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background
methodsThe study was conducted in Aurangabad (India) from 16 February to 10 June 2015. CGME treated MCF-7 cells were analyzed for growth inhibition and apoptosis. The exhibition of phosphatidylserine was analyzed with the Annexin-V Fluorescein isothiocyanate flow cytometry (FITC) method. Accumulated poly-caspases were determined with carboxyfluorescein poly-caspase assay, Apo-BrdU™ tunnel assay for DNA fragmentation and pro/anti-apoptotic gene expression with real-time polymerase chain reaction. The high-performance liquid chromatography analysis indicated the presence of two unknown cardenolides along with known cardenolides such as calactin, calatropagenin, usharin, afroside, calatoxin, and gamphoside. The Kruskal-Wallis and Wilcoxon tests (GraphPad Prism version 7.0) were used for statistical analyses.
resultsUpon treatment with 40 µg/ml CGME, about 56.9% of the cell population underwent apoptosis. Compared to paclitaxel, the accumulation of active caspases in CGME treated with MCF-7 cells was found to be dose-dependent, whereas the G2/M cell cycle arrest was time-dependent. The Apo-BrdU™ tunnel assay confirmed that CGME treatment caused DNA fragmentation and RT-PCR analyses indicated elevated transcription for pro-apoptotic gene expression. Kruskal-Wallis test results were significant; Bcl-2 (P=0.00193), Bak-1 (P=0.00021), and Bax (P=0.0019).
conclusionCGME treatment caused the accumulation of phosphatidylserine on the cell membrane, recruitment of poly-caspases, DNA fragmentation, and enhanced transcription of pro-apoptotic gene expression.
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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.