ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
Investigation of the sensitivity of human A549 cells to paclitaxel and sesquiterpene lactone alantolactone via apoptosis induction.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Identification and experimental validation of biomarkers associated with integrated stress response in sepsis.Biochemistry and biophysics reports · 2026Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alantolactone (ALA), a sesquiterpene lactone compound obtained from Inula helenium root, is known to have anticancer activity in many types of cancer. Paclitaxel (PAX) is an effective first-line chemotherapeutic drug and is widely used in the treatment of lung cancer. The in vitro anticancer efficacy of combined treatment of ALA with PAX was investigated in the A549 human lung cancer cell line. The results show that ALA potentiated the effect of PAX-induced growth restriction and apoptosis in A549 cells. The combined administration more effectively decreased the Bcl-2 expression and increased Bax gene expression in cells compared to ALA or PAX alone. Also, co-treatment of ALA and PAX caused apoptotic nuclear formations. Additionally, coadministration increased the caspase-3 and caspase-9 levels more than PAX or ALA alone. The increase in NF-κB gene expression levels suggests that an NF-κB-independent apoptotic trigger mechanism operates in cells. Together, the present in vitro findings suggest that ALA may contribute as a potential therapeutic strategy in the treatment of lung cancer.
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Registered trials
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