ArticleIn vivo (Athens, Greece)
Lauryl Gallate Induces Apoptotic Cell Death through Caspase-dependent Pathway in U87 Human Glioblastoma Cells
Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 8 citations in OpenAlex.
- Characterization of ficus hispida fruit extract and assessment of Gallic acid using in Silico and in vitro studies against breast cancer.Scientific reports · 2025Article
- Magnolol Induces the Extrinsic/Intrinsic Apoptosis Pathways and Inhibits STAT3 Signaling-Mediated Invasion of Glioblastoma Cells.Life (Basel, Switzerland) · 2021Article
- Gallic acid-gold nanoparticles enhance radiation-induced cell death of human glioma U251 cells.IUBMB life · 2021Article
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Authors and funding
7 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimThe treatment of human glioma tumor is still an unmet medical need. Natural products are always promising resources for discovery of anticancer drugs. Lauryl gallate (LG) is one of the derivatives of gallic acid, widely present in plants, that has been shown to induce anticancer activities in many human cancer cell lines; however, it has not been studied in human glioma cell lines. Thus, the effects of LG on human glioblastoma U87 cells were investigated in the present in vitro study. MATERIALS AND
methodsCell morphology and viability were examined by phase-contrast microscopy. Annexin V/Propidium iodide (PI) double staining were performed and assayed by flow cytometry to confirm that viable cell number reduction was due to the induction of apoptosis. Furthermore, U87 cells were exposed to LG in various concentrations and were analyzed by caspase activity assay. To further confirm that LG induced apoptotic cell death, the expression of apoptosis-associated proteins in LG-treated U87 cells was tested by western blot.
resultsLG induced morphological changes and decreased viability in U87 cells. Annexin V/PI double staining revealed that LG induced apoptotic cell death in U87 cells in a dose-dependent manner. The increased activities of caspase-2, -3, -8 and -9 demonstrated that LG induced U87 cell apoptosis through a caspase-dependent pathway. In terms of molecular level, LG increased pro-apoptotic proteins Bax and Bak and decreased anti-apoptotic protein Bcl-2 in U87 cells. Furthermore, LG also suppressed the expression of p-Akt, Pak1, Hif-1α and Hif-2α, β-catenin and Tcf-1 in U87 cells.
conclusionThese results suggest that LG induced apoptotic cell death via the caspase-dependent pathway in U87 cells.
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