Data supporting the inability of indomethacin to induce autophagy in U251 glioma cells
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Updated: Mar 7, 2026
Quantitative Analysis of Autophagy using Advanced 3D Fluorescence Microscopy
Published on: May 3, 2013
Aleksandar Pantovic1, Katarina Arsikin2, Milica Kosic2
1Neurology Clinic, Military Medical Academy, Belgrade, Serbia.
Abstract:
Autophagy, a catabolic process involving intracellular degradation of unnecessary or dysfunctional cellular components through the lysosomal machinery, could act as a prosurvival, as well as a cytotoxic mechanism (Parzych and Klionsky, 2014) [1]. Cyclooxygenase inhibitor indomethacin inhibits proliferation of glioma cells, and has been reported to reduce the activity of the main autophagy repressor mammalian target of rapamycin (mTOR) (Pantovic et al., 2016) [2]. Here we investigated the ability of indomethacin to induce autophagy in U251 human glioma cells. We assessed the influence of indomethacin on intracellular acidification, expression of proautophagic protein beclin-1, and conversion of microtubule-associated protein light chain 3-I (LC3-I) to autophagosome-associated LC3-II, in the presence or absence of lysosomal inhibitors. The effect of genetic and pharmacological downregulation of autophagy on the cytotoxicity of indomethacin was also evaluated. The interpretation of these data can be found in "In vitro antiglioma action of indomethacin is mediated via AMP-activated protein kinase/mTOR complex 1 signaling pathway" (Pantovic et al., 2016; doi:10.1016/j.biocel.2016.12.007) [2].
Insights
Indomethacin, a cyclooxygenase inhibitor, triggers autophagy in glioma cells. This process influences cell death, suggesting potential therapeutic strategies for brain tumors.
Area of Science:
- Cell Biology
- Molecular Biology
- Cancer Research
Background:
- Autophagy is a cellular degradation process with dual roles in cell survival and death.
- Indomethacin, a cyclooxygenase inhibitor, has shown antiproliferative effects on glioma cells.
- Mammalian target of rapamycin (mTOR), a key autophagy repressor, is inhibited by indomethacin.
Purpose of the Study:
- To investigate the ability of indomethacin to induce autophagy in U251 human glioma cells.
- To assess the impact of indomethacin on key autophagy markers and intracellular acidification.
- To evaluate the role of autophagy modulation in indomethacin-induced glioma cell cytotoxicity.
Main Methods:
- U251 human glioma cells were treated with indomethacin.
- Intracellular acidification, beclin-1 expression, and LC3-I to LC3-II conversion were measured.
- Autophagy was genetically and pharmacologically downregulated to assess its effect on indomethacin cytotoxicity.
Main Results:
- Indomethacin induced autophagy in U251 human glioma cells.
- The drug affected intracellular acidification and key autophagy-related protein expression.
- Downregulation of autophagy influenced the cytotoxic effects of indomethacin on glioma cells.
Conclusions:
- Indomethacin-induced autophagy plays a role in the anti-glioma activity of the drug.
- Modulating autophagy in conjunction with indomethacin may offer therapeutic potential for glioma treatment.
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