›› 2019, Vol. 39 ›› Issue (8): 848-.doi: 10.3969/j.issn.1674-8115.2019.08.007

• Original article (Basic research) • Previous Articles     Next Articles

Regulation of mitochondrial carrier SLC25A13 on breast cancer cell cycle in vitro

GU Xiao-ping1, CHEN Meng-ping1, LIANG A-juan2, LIU Yun-xia1, SUN Hai-peng1, HUANG Ying1   

  1. 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, Shanghai 200025, China; 2. Center for Reproductive Medicine, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China.
  • Online:2019-08-28 Published:2019-09-23
  • Supported by:
    Morning Star Prograrm of Shanghai Municipal Science and Technology Commission, 11QA1403700; Shanghai College Experimental Technology Team Building Plan; K.C. Wong Medical Fellowship Fund, Shanghai Jiao Tong University

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Abstract: Objective · To investigate the role of mitochondrial solute carrier family 25 member 13 (SLC25A13) on breast cancer development. Methods · SLC25A13 mRNA and protein s in invasive breast cancer tissues and normal breast tissues were The Cancer Genome Atlas (TCGA) breast cancer dataset. Survival analysis was conducted onlineKaplan-Meier software. MCF-7 cell line was used for in vitro cell assay. Knockdown of SLC25A13 and sirtuin 2 (SIRT2) were conductedsiRNA transfection. Cell viability was measured with trypan blue exclusion. Cell cycle arrest was determinedflow cytometry. The mRNA of SLC25A13 and P27 were detectedquantitative PCR. The protein level of SLC25A13, P27 and SIRT2 were detectedWestern blotting. Protein half-life of P27 was assessedWestern blotting after cycloheximide treatment. Results · SLC25A13 was up-regulated in invasive breast cancer tissues. High 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 prolonged protein half-life. Knockdown of SIRT2 restored cell cycle arrest as well as P27 accumulation causedSLC25A13 silencing. Conclusion · High of SLC25A13 may promote cell cycle progression via SIRT2 in breast cancer development.

Key words: solute carrier family 25 member 13 (SLC25A13), sirtuin-2 (SIRT2), P27, breast cancer, cell cycle

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