ArticleCellular and molecular life sciences : CMLS2009
Doxorubicin-mediated apoptosis in glioma cells requires NFAT3.
Article in Cellular and molecular life sciences : CMLS, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Dual-targeted glutathione-glutamate functionalized Bismuth-Niosomes hybrid nanosystem for co-delivery of doxorubicin and Pi3K inhibitor into U87 glioblastoma cells.Scientific reports · 2026Article
- Recent knowledge of NFATc4 in oncogenesis and cancer prognosis.Cancer cell international · 2022Review
- Specific Compositions ofCancers · 2021Article
- Expression, Prognosis and Gene Regulation Network of NFAT Transcription Factors in Non-Small Cell Lung Cancer.Pathology oncology research : POR · 2021Article
- Article
- Nfatc4 Deficiency Attenuates Ototoxicity by Suppressing Tnf-Mediated Hair Cell Apoptosis in the Mouse Cochlea.Frontiers in immunology · 2019Article
- Prophylactic supplementation of resveratrol is more effective than its therapeutic use against doxorubicin induced cardiotoxicity.PloS one · 2017Article
- DT(270-326) , a Truncated Diphtheria Toxin, Increases Blood-Tumor Barrier Permeability by Upregulating the Expression of Caveolin-1.CNS neuroscience & therapeutics · 2016Article
- Altered expression of long non-coding RNAs during genotoxic stress-induced cell death in human glioma cells.Journal of neuro-oncology · 2015Article
- Role of methamphetamine on glioblastoma cytotoxicity induced by doxorubicin and methotrexate.Neurotoxicity research · 2014Article
- Loss of PDCD4 contributes to enhanced chemoresistance in Glioblastoma multiforme through de-repression of Bcl-xL translation.Oncotarget · 2013Article
- PMA and ionomycin induce glioblastoma cell death: activation-induced cell-death-like phenomena occur in glioma cells.PloS one · 2013Article
- Regulator of G protein signaling 6 mediates doxorubicin-induced ATM and p53 activation by a reactive oxygen species-dependent mechanism.Cancer research · 2011Article
- Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Nuclear factor of activated T cells (NFAT), a family of transcription factors, has been implicated in many cellular processes, including some cancers. Here, we characterize, for the first time, the role of NFAT3 in doxorubicin (DOX)-mediated apoptosis, migration, and invasion in SNB19 and U87 glioma cells. This study demonstrates that the specific knockdown of NFAT3 results in a dramatic inhibition of the apoptotic effect induced by DOX and favors cell survival. Inhibition of NFAT3 activation by shNFAT3 (shNF3) significantly downregulated tumor necrosis factor (TNF)-alpha induction, its receptor TNFR1, caspase 10, caspase 3, and poly (ADP-ribose) polymerase, abrogating DOX-mediated apoptosis in glioma cells. DOX treatment resulted in NFAT3 translocation to the nucleus. Similarly, shNF3 treatment in SNB19 and U87 cells reversed DOX-induced inhibition of cell migration and invasion, as determined by wound healing and matrigel invasion assays. Taken together, these results indicate that NFAT3 is a prerequisite for the induction of DOX-mediated apoptosis in glioma cells.
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