Mitochondrial Fission Protein 1 (FIS1) Overexpression in Human Cervical Cancer Cells Promotes Mitochondrial Fission and Reduces Cell Proliferation and Migration Capacity
10.13865/j.cnki.cjbmb.2022.05.1024
- Author:
Rui CONG
1
;
Xing-Yu LI
1
;
Nan HUO
1
;
Xiang ZHU
1
;
Chun-Yuan XUE
1
;
Liao-Xin FANG
1
;
Xiao-Feng KANG
1
;
Jun-Wen ZHU
1
;
Yi-Meng DU
1
;
Xiao-Jie XU
1
Author Information
1. Department of Cellular Engineering, Beijing Institute of Biotechnology
- Publication Type:Journal Article
- Keywords:
bioinformatics;
cervical cancer;
mitochondria;
mitochondrial fission protein 1 (FIS1);
The Cancer Genome Atlas (TCGA)
- From:
Chinese Journal of Biochemistry and Molecular Biology
2022;38(7):926-935
- CountryChina
- Language:Chinese
-
Abstract:
Mitochondria are dynamic organelles that continuously divide and fuse. In recent years, in addition to the studies related to mitochondrial metabolism, the unique dynamics of mitochondria have gradually attracted researchers' attention. A growing body of research has revealed that mitochondrial dynamics are related to the biological behavior of tumor cells. Mitochondrial fission proteins (mitochondrial fission protein 1, FIS1) mediate the assembly of mitochondrial fission complexes and participate in the execution of mitochondrial fission. They are important proteins in the process of mitochondrial fusion and fission. However, few studies have revealed the expression and role of FIS1 in human cervical cancer. In this study, the expression level of FIS1 in human cervical cancer tissues and paracancer tissues were compared. The results showed that the level of FIS1 mRNA in human cervical cancer tissues was significantly lower than that in paracancer tissues (P<0. 01). Further KEGG pathway and GO Term-BP pathway analysis showed that the differential genes are mainly related to mitochondrial biological functions. Subsequently, HeLa cells with overexpressed FIS1 were investigated for their proliferation, migration, mitochondrial fission and ROS levels. The experimental results showed that FIS1 overexpression decreased HeLa cell proliferation and migration ability, enhanced mitochondrial fission and higher ROS levels. In conclusion, the expression of FIS1 in human cervical cancer cells was attenuated, while overexpression of FIS1 resulted in a series of abnormal biological functions in human cervical cancer cells. Further studies can be carried out to investigate the role of FIS1 in the treatment of human cervical cancer.
