ArticleCancer cell international2021
EF24 exerts cytotoxicity against NSCLC via inducing ROS accumulation.
Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Article
- Bioactive components and delivery strategies of food-medicine homologous substances in lung cancer therapy: current advances and clinical translation.Frontiers in nutrition · 2025Review
- Antioxidant curcumin induces oxidative stress to kill tumor cells (Review).Oncology letters · 2024Review
- Review
- Curcumin and Its Analogs in Non-Small Cell Lung Cancer Treatment: Challenges and Expectations.Biomolecules · 2022Review
- Regulation of apoptosis, autophagy and ferroptosis by non-coding RNAs in metastatic non-small cell lung cancer (Review).Experimental and therapeutic medicine · 2022Review
- Targeted Pyroptosis Is a Potential Therapeutic Strategy for Cancer.Journal of oncology · 2022Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe role of Diphenyldifluoroketone (EF24), a synthetic analogue of curcumin with noteworthy antitumor potential, remains unclear in non-small cell lung cancer (NSCLC). Herein, the inhibitory effect of EF24 on NSCLC and its mechanism were studied.
methodsCytotoxicity was measured by MTT assay, colony formation assay and xenograft model. Cell apoptosis and reactive oxygen species (ROS) level were quantified by flow cytometer. Protein level was detected by western blot assay. Mitochondria and autophagosomes were observed using transmission electron microscope and confocal microscopy.
resultsIn-vitro, EF24 significantly induced proliferation inhibition, apoptosis, mitochondrial fission and autophagy of NSCLC cell lines. These cytotoxic effects were significantly attenuated by two reactive oxygen species (ROS) scavengers, indicating its anti-cancer effects largely depend on ROS accumulation. In-vivo, EF24 inhibited tumor growth in a dose-dependent manner. Moreover, no pathological changes of heart, lung, spleen, kidney and liver of mice were observed. Collectively, EF24 induced ROS accumulation, in turn activates cell apoptosis, and then exerts its cytotoxicity on NSCLC cells.
conclusionsThe results showed that EF24 exerted cytotoxicity against NSCLC via ROS accumulation. Thus, EF24 might serve as a potential anti-cancer agent for the treatment of NSCLC.
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