期刊
MOLECULAR MEDICINE REPORTS
卷 19, 期 1, 页码 271-279出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2018.9644
关键词
hypoxia; microRNA-210; Kruppel-like factor 7; apoptosis; mouse spermatocyte GC-2 cells
资金
- Key Discipline of Medicine of Jiangsu Province [ZDXKA2016012]
- Suzhou Key Medical Center [SZXK2015020, SZZXJ201501]
- Suzhou Government [LCZX201502, SYS201754]
- National Natural Science Foundation of China [81300537]
The aim of the present study was to investigate the underlying mechanisms of hypoxia-induced microRNA (miR)-210 effects on mouse GC-2spd (GC-2) cells. GC-2 cells were subjected to hypoxia or normoxia for 12, 24, 48 and 72 h. Apoptosis of GC-2 cells was detected using terminal deoxynucleotidyl-transferase-meditated dUTP nick end labeling and flow cytometry. Reverse transcription-quantitative polymerase chain reaction was performed to analyze the expression of miR-210. Hypoxia-inducible factor-1 (HIF-1), caspase-3, B-cell lymphoma 2, apoptosis regulator BAX and Kruppel-like factor 7 (KLF7) protein expression levels were detected by western blotting. Luciferase reporter gene assays were used to assess the targeting effects of miR-210 on KLF7. Hypoxia induced GC-2 cell apoptosis and increased the expression of HIF-1 and pro-apoptotic proteins; however, decreased anti-apoptotic protein expression levels. Furthermore, hypoxia resulted in the upregulation of miR-210 in GC-2 cells. HIF-1 and miR-210 were involved in the apoptosis of GC-2 cells by mediating the expression of apoptosis-associated proteins. Furthermore, KLF7 was directly targeted by miR-210 to influence the apoptosis of GC-2 cells subjected to hypoxia. The results suggested that hypoxia-induced miR-210 stimulated the activation of the apoptosis signaling pathway and contributed to the apoptosis of GC-2 cells by targeting KLF7.
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