Data supporting the inability of indomethacin to induce autophagy in U251 glioma cells

Publication date: Available online 10 February 2017
Source:Data in Brief
Author(s): Aleksandar Pantovic, Katarina Arsikin, Milica Kosic, Biljana Ristic, Vladimir Trajkovic, Ljubica Harhaji-Trajkovic
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 [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) [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 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 signalling pathway" (Pantovic et al. 2017; doi:10.1016/j.biocel.2016.12.007) [2].



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