scholarly journals Sentrin/small ubiquitin-like modifier-specific protease 5 protects oral cancer cells from oxidative stress-induced apoptosis

2015 ◽  
Vol 12 (2) ◽  
pp. 2009-2014 ◽  
Author(s):  
YONG CHENG ◽  
XUEHUA GUO ◽  
YIMING GONG ◽  
XIAOJUN DING ◽  
YOUCHENG YU
2009 ◽  
Vol 47 (3) ◽  
pp. 561-570 ◽  
Author(s):  
H.-Z. Lee ◽  
W.-Z. Liu ◽  
W.-T. Hsieh ◽  
F.-Y. Tang ◽  
J.-G. Chung ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Jing-Iong Yang ◽  
Jen-Yang Tang ◽  
Ya-Sin Liu ◽  
Hui-Ru Wang ◽  
Sheng-Yang Lee ◽  
...  

Roe protein hydrolysates were reported to have antioxidant property but the anticancer effects were less addressed, especially for oral cancer. In this study, we firstly used the ultrafiltrated roe hydrolysates (URH) derived from giant grouper (Epinephelus lanceolatus) to evaluate the impact of URH on proliferation against oral cancer cells. We found that URH dose-responsively reduced cell viability of two oral cancer cells (Ca9-22 and CAL 27) in terms of ATP assay. Using flow cytometry, URH-induced apoptosis of Ca9-22 cells was validated by morphological features of apoptosis, sub-G1 accumulation, and annexin V staining in dose-responsive manners. URH also induced oxidative stress in Ca9-22 cells in terms of reactive oxygen species (ROS)/superoxide generations and mitochondrial depolarization. Taken together, these data suggest that URH is a potential natural product for antioral cancer therapy.


Antioxidants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1588
Author(s):  
Su-Ling Liu ◽  
Kun-Han Yang ◽  
Che-Wei Yang ◽  
Min-Yu Lee ◽  
Ya-Ting Chuang ◽  
...  

Burmannic acid (BURA) is a new apocarotenoid bioactive compound derived from Indonesian cinnamon; however, its anticancer effect has rarely been investigated in oral cancer cells. In this investigation, the consequences of the antiproliferation of oral cancer cells effected by BURA were evaluated. BURA selectively suppressed cell proliferation of oral cancer cells (Ca9-22 and CAL 27) but showed little cytotoxicity to normal oral cells (HGF-1). In terms of mechanism, BURA perturbed cell cycle distribution, upregulated mitochondrial superoxide, induced mitochondrial depolarization, triggered γH2AX and 8-hydroxy-2-deoxyguanosine DNA damage, and induced apoptosis and caspase 3/8/9 activation in oral cancer cells. Application of N-acetylcysteine confirmed oxidative stress as the critical factor in promoting antiproliferation, apoptosis, and DNA damage in oral cancer cells.


2020 ◽  
Vol 19 ◽  
pp. 877-889 ◽  
Author(s):  
Ming-Ju Hsieh ◽  
Chiao-Wen Lin ◽  
Shih-Chi Su ◽  
Russel J. Reiter ◽  
Andy Wei-Ge Chen ◽  
...  

2017 ◽  
Vol 73 ◽  
pp. 1-6 ◽  
Author(s):  
Lee-Han Kim ◽  
Ji-Ae Shin ◽  
Boonsil Jang ◽  
In-Hyoung Yang ◽  
Dong-Hoon Won ◽  
...  

Antioxidants ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 694
Author(s):  
Jen-Yang Tang ◽  
Kuang-Han Wu ◽  
Yen-Yun Wang ◽  
Ammad Ahmad Farooqi ◽  
Hurng-Wern Huang ◽  
...  

Some lichens provide the resources of common traditional medicines and show anticancer effects. However, the anticancer effect of Usnproliea barbata (U. barbata) is rarely investigated, especially for oral cancer cells. The aim of this study was to investigate the cell killing function of methanol extracts of U. barbata (MEUB) against oral cancer cells. MEUB shows preferential killing against a number of oral cancer cell lines (Ca9-22, OECM-1, CAL 27, HSC3, and SCC9) but rarely affects normal oral cell lines (HGF-1). Ca9-22 and OECM-1 cells display the highest sensitivity to MEUB and were chosen for concentration effect and time course experiments to address its cytotoxic mechanisms. MEUB induces apoptosis of oral cancer cells in terms of the findings from flow cytometric assays and Western blotting, such as subG1 accumulation, annexin V detection, and pancaspase activation as well as poly (ADP-ribose) polymerase (PARP) cleavage. MEUB induces oxidative stress and DNA damage of oral cancer cells following flow cytometric assays, such as reactive oxygen species (ROS)/mitochondrial superoxide (MitoSOX) production, mitochondrial membrane potential (MMP) depletion as well as overexpression of γH2AX and 8-oxo-2′deoxyguanosine (8-oxodG). All MEUB-induced changes in oral cancer cells were triggered by oxidative stress which was validated by pretreatment with antioxidant N-acetylcysteine (NAC). In conclusion, MEUB causes preferential killing of oral cancer cells and is associated with oxidative stress, apoptosis, and DNA damage.


2017 ◽  
Vol 8 ◽  
Author(s):  
Hsueh-Wei Chang ◽  
Ruei-Nian Li ◽  
Hui-Ru Wang ◽  
Jing-Ru Liu ◽  
Jen-Yang Tang ◽  
...  

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