Hypoxia‑induced miR‑210 contributes to apoptosis of mouse spermatocyte GC‑2 cells by targeting Kruppel‑like factor 7

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‑1α (HIF‑1α), 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‑1α 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‑1α 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.