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O-GlcNAcylation mediates H2O2-induced apoptosis through regulation of STAT3 and FOXO1

  
@article{APS11000,
	author = {Chen-chun Zhang and Yuan Li and Chang-you Jiang and Qiu-min Le and Xing Liu and Lan Ma and Fei-fei Wang},
	title = {O-GlcNAcylation mediates H 2 O 2 -induced apoptosis through regulation of STAT3 and FOXO1},
	journal = {Acta Pharmacologica Sinica},
	volume = {45},
	number = {4},
	year = {2024},
	keywords = {},
	abstract = {The O-linked-β-N-acetylglucosamine (O-GlcNAc) glycosylation (O-GlcNAcylation) is a critical post-translational modification that couples the external stimuli to intracellular signal transduction networks. However, the critical protein targets of O-GlcNAcylation in oxidative stress-induced apoptosis remain to be elucidated. Here, we show that treatment with H2O2 inhibited O-GlcNAcylation, impaired cell viability, increased the cleaved caspase 3 and accelerated apoptosis of neuroblastoma N2a cells. The O-GlcNAc transferase (OGT) inhibitor OSMI-1 or the O-GlcNAcase (OGA) inhibitor Thiamet-G enhanced or inhibited H2O2-induced apoptosis, respectively. The total and phosphorylated protein levels, as well as the promoter activities of signal transducer and activator of transcription factor 3 (STAT3) and Forkhead box protein O 1 (FOXO1) were suppressed by OSMI-1. In contrast, overexpressing OGT or treating with Thiamet-G increased the total protein levels of STAT3 and FOXO1. Overexpression of STAT3 or FOXO1 abolished OSMI-1-induced apoptosis. Whereas the anti-apoptotic effect of OGT and Thiamet-G in H2O2-treated cells was abolished by either downregulating the expression or activity of endogenous STAT3 or FOXO1. These results suggest that STAT3 or FOXO1 are the potential targets of O-GlcNAcylation involved in the H2O2-induced apoptosis of N2a cells.},
	issn = {1745-7254},	url = {http://www.chinaphar.com/article/view/11000}
}