Regulation of mitochondrial carrier slc25a13 on breast cancer cell cycle in vitro
10.3969/j.issn.1674-8115.2019.08.007
- Author:
Xiao-Ping GU
1
Author Information
1. Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University College of Basic Medical Sciences
- Publication Type:Journal Article
- Keywords:
Breast cancer;
Cell cycle;
P27;
Sirtuin-2 (SIRT2);
Solute carrier family 25 member 13 (SLC25A13)
- From:
Journal of Shanghai Jiaotong University(Medical Science)
2019;39(8):848-855
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the role of mitochondrial solute carrier family 25 member 13 (SLC25A13) on breast cancer development. Methods:SLC25A13 mRNA and protein expressions in invasive breast cancer tissues and normal breast tissues were from The Cancer Genome Atlas (TCGA) breast cancer dataset. Survival analysis was conducted online by Kaplan-Meier software. MCF-7 cell line was used for in vitro cell assay. Knockdown of SLC25A13 and sirtuin 2 (SIRT2) were conducted by siRNA transfection. Cell viability was measured with trypan blue exclusion. Cell cycle arrest was determined by flow cytometry. The mRNA expression of SLC25A13 and P27 were detected by quantitative PCR. The protein level of SLC25A13, P27 and SIRT2 were detected by Western blotting. Protein half-life of P27 was assessed by Western blotting after cycloheximide treatment. Results:SLC25A13 was up-regulated in invasive breast cancer tissues. High expression of SLC25A13 correlated with poor overall survival and breast cancer recurrence. SLC25A13 knockdown inhibited MCF-7 cell cycle progression. P27 and SIRT2 both accumulated after SLC25A13 knockdown. P27 accumulation resulted from prolonged protein half-life. Knockdown of SIRT2 restored cell cycle arrest as well as P27 accumulation caused by SLC25A13 silencing. Conclusion:High expression of SLC25A13 may promote cell cycle progression via SIRT2 in breast cancer development.
