Data supporting the inability of indomethacin to induce autophagy in U251 glioma cells
2017
Authors:
Pantović, AleksandarArsikin, Katarina
Kosić, Milica
Risti, Biljana
Trajkovi, Vladimir
Harhaji-Trajković, Ljubica
Document Type:
Article (Published version)
Metadata
Show full item recordAbstract:
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].
Keywords:
Autophagy; Beclin-1; Glioma; Indomethacin; LC3Funding / projects:
- The role of autophagy in regulation of cancer cell death (RS-MESTD-Basic Research (BR or ON)-173053)
- Modulation of intracellular energy balance-controlling signalling pathways in therapy of cancer and neuro-immuno-endocrine disorders (RS-MESTD-Integrated and Interdisciplinary Research (IIR or III)-41025)
In:
- Data in Brief (2017), 11: 225-230
DOI: 10.1016/j.dib.2017.02.012
ISSN: 2352-3409
PubMed: 28243617
Scopus: 2-s2.0-85013367791
URI
http://www.sciencedirect.com/science/article/pii/S2352340917300318http://www.ncbi.nlm.nih.gov/pubmed/28243617
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC5320059
https://radar.ibiss.bg.ac.rs/handle/123456789/2585