Sentrin/small ubiquitin-like modifier-specific protease 5 protects oral cancer cells from oxidative stress-induced apoptosis
The aim of the present study was to investigate the role of sentrin/small ubiquitin-like modifier (SUMO)-specific protease 5 (SENP5) in oral squamous cell carcinoma (OSCC), as the overexpression of SENP5 has been observed in 31 OSCC tissue specimens. CAL27 OSCC cells were used for in vitro measurements. The distribution of SENP5 was visualized using immunohistochemistry and H2O2induced oxidative stress, and the effects of SENPsmall interfering RNA on SENP5 were analyzed via western blotting. The apoptotic rates of the CAL27 cells during oxidative stress and SENP5 silencing were estimated using flowcytometry, and the mitochondrial structures were analyzed using a mitochondria tracker. The SENP5 protein was localized in the nuclei and cytosols of the CAL27 cells, and incubation with 100 µm H2O2 for >1 h led to its stabilization. Incubation with H2O2 alone had no effect on the CAL27 cells, however, a combination of H2O2 and SENP5 silencing led to enhanced apoptotic rates (P<0.001). Analysis of the mitochondrial structures revealed that H2O2 alone enhanced mitochondrial network formation, whereas the combination of H2O2 and SENP5 silencing led to mitochondrial fragmentation in the CAL27 cells. The overexpression of SENP5 partly localized in the cytosol of the OSCC cells. Mild oxidative stress stabilized the SENP5 protein in the CAL27 cells, and only the combination of SENP5 silencing and H2O2 application led to mitochondria fragmentation and a significant increase in cell apoptosis. Therefore, SENP5 protected the OSCC cells from oxidative stress-induced apoptosis.
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Document Type: Research Article
Affiliations: Department of Stomatology, Zhongshan Hospital of Fudan University, Shanghai 200032, P.R. China
Publication date: August 1, 2015
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