TY  - JOUR
AU  - Pantović, Aleksandar
AU  - Arsikin, Katarina
AU  - Kosić, Milica
AU  - Risti, Biljana
AU  - Trajkovi, Vladimir
AU  - Harhaji-Trajković, Ljubica
PY  - 2017
UR  - http://www.sciencedirect.com/science/article/pii/S2352340917300318
UR  - http://www.ncbi.nlm.nih.gov/pubmed/28243617
UR  - http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC5320059
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2585
AB  - 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].
T2  - Data in Brief
T1  - Data supporting the inability of indomethacin to induce autophagy in U251 glioma cells
VL  - 11
DO  - 10.1016/j.dib.2017.02.012
SP  - 225
EP  - 230
ER  - 

@article{
author = "Pantović, Aleksandar and Arsikin, Katarina and Kosić, Milica and Risti, Biljana and Trajkovi, Vladimir and Harhaji-Trajković, Ljubica",
year = "2017",
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].",
journal = "Data in Brief",
title = "Data supporting the inability of indomethacin to induce autophagy in U251 glioma cells",
volume = "11",
doi = "10.1016/j.dib.2017.02.012",
pages = "225-230"
}

Pantović, A., Arsikin, K., Kosić, M., Risti, B., Trajkovi, V.,& Harhaji-Trajković, L.. (2017). Data supporting the inability of indomethacin to induce autophagy in U251 glioma cells. in Data in Brief, 11, 225-230.
https://doi.org/10.1016/j.dib.2017.02.012

Pantović A, Arsikin K, Kosić M, Risti B, Trajkovi V, Harhaji-Trajković L. Data supporting the inability of indomethacin to induce autophagy in U251 glioma cells. in Data in Brief. 2017;11:225-230.
doi:10.1016/j.dib.2017.02.012 .

Pantović, Aleksandar, Arsikin, Katarina, Kosić, Milica, Risti, Biljana, Trajkovi, Vladimir, Harhaji-Trajković, Ljubica, "Data supporting the inability of indomethacin to induce autophagy in U251 glioma cells" in Data in Brief, 11 (2017):225-230,
https://doi.org/10.1016/j.dib.2017.02.012 . .