上海交通大学学报(医学版) ›› 2019, Vol. 39 ›› Issue (8): 848-.doi: 10.3969/j.issn.1674-8115.2019.08.007
GU Xiao-ping1, CHEN Meng-ping1, LIANG A-juan2, LIU Yun-xia1, SUN Hai-peng1, HUANG Ying1
GU Xiao-ping1, CHEN Meng-ping1, LIANG A-juan2, LIU Yun-xia1, SUN Hai-peng1, HUANG Ying1
摘要: 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.
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