Oxaliplatin induces the PARP1-mediated parthanatos in oral squamous cell carcinoma by increasing production of ROS

被引:2
作者
Li, Dongfang [1 ,2 ,3 ]
Kou, Yuying [1 ,2 ,3 ]
Gao, Yuan [1 ,2 ,3 ]
Liu, Shanshan [1 ,2 ,3 ]
Yang, Panpan [1 ,2 ,3 ]
Hasegawa, Tomoka [4 ]
Su, Rongjian [5 ]
Guo, Jie [1 ,2 ,3 ]
Li, Minqi [1 ,2 ,3 ]
机构
[1] Shandong Univ, Sch & Hosp Stomatol, Cheeloo Coll Med, Dept Bone Metab, Jinan 250012, Peoples R China
[2] Shandong Key Lab Oral Tissue Regenerat, Jinan 250012, Peoples R China
[3] Shandong Engn Lab Dent Mat & Oral Tissue Regenera, Jinan 250012, Peoples R China
[4] Hokkaido Univ, Grad Sch Dent Med, Dept Dev Biol Hard Tissue, Sapporo, Hokkaido 0608586, Japan
[5] Jinzhou Med Univ, Life Sci Inst, Coll Basic Med,Educ Dept Liaoning Prov, Cell Biol & Genet Dept,Key Lab Mol & Cellular Bio, Jinzhou 121001, Peoples R China
来源
AGING-US | 2021年 / 13卷 / 03期
关键词
oxaliplatin; parthanatos; oral squamous cell carcinoma; ROS; OXIDATIVE STRESS; CANCER STATISTICS; PARP INHIBITORS; GLIOMA-CELLS; ACTIVATION; DEATH; MECHANISMS; RESISTANT; EFFICACY;
D O I
暂无
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Oral squamous cell carcinoma (OSCC) is one of the most common malignant tumors worldwide, and its prognosis is still not optimistic. Oxaliplatin is a type of platinum chemotherapeutic agent, but its treatment effects on OSCC and molecular mechanisms have not been fully elucidated. Parthanatos, a unique form of cell death, plays an important role in a variety of physiological and pathological processes. This study aims to investigate whether oxaliplatin inhibits OSCC by inducing parthanatos. Our results showed that oxaliplatin inhibited the proliferation and migration of OSCC cells in vitro, and also inhibited the tumorigenesis in vivo. Further experiments proved that oxaliplatin induced parthanatos in OSCC cells, characterized by depolarization of the mitochondrial membrane potential, up-regulation of PARP1, AIF and MIF in the nucleus, as well as the nuclear translocation of AIF. Meanwhile, PARP1 inhibitor rucaparib and siRNA against PARP1 attenuated oxaliplatin-induced parthanatos in OSCC cells. In addition, we found that oxaliplatin caused oxidative stress in OSCC cells, and antioxidant NAC not only relieved oxaliplatin-induced overproduction of reactive oxygen species (ROS) but also reversed parthanatos caused by oxaliplatin. In conclusion, our results indicate that oxaliplatin inhibits OSCC by activating PARP1-mediated parthanatos through increasing the production of ROS.
引用
收藏
页码:4242 / 4257
页数:16
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