FOXG1 improves mitochondrial function and promotes the progression of nasopharyngeal carcinoma

Forkhead‑box gene 1 (FOXG1) has been reported to serve an important role in various malignancies, but its effects on nasopharyngeal cancer (NPC) remain unknown. Thus, the present study aimed to investigate the specific regulatory relationship between FOXG1 and NPC progression. Tumor tissues and matching para‑carcinoma tissues were obtained from patients with NPC. Small interfering (si)RNA‑FOXG1 and pcDNA3.1‑FOXG1 were transfected into SUNE‑1 and C666‑1 cells to knockdown and overexpress FOXG1 expression, respectively. FOXG1 expression was detected using reverse transcription‑quantitative PCR and immunohistochemistry. Cell proliferation was detected using MTT and 5‑ethynyl‑20‑deoxyuridine assays. Transwell invasion assay, wound healing assay and flow cytometry were used to detect cell invasion, migration and apoptosis, respectively. Western blotting was conducted to detect the expression levels of mitochondrial markers (succinate dehydrogenase complex flavoprotein subunit A, heat shock protein 60 and pyruvate dehydrogenase), epithelial‑mesenchymal transition (EMT) related proteins (N‑cadherin, Snail and E‑cadherin) and apoptosis‑related proteins [Bax, Bcl‑2, poly(ADP‑ribose) polymerase 1 (PARP), cleaved PARP, cleaved caspase‑3, cleaved caspase‑8, cleaved caspase‑9, caspase‑3, caspase‑8 and caspase‑9]. The mitochondrial membrane potential was detected via flow cytometry, while the ATP/ADP ratio was determined using the ADP/ATP ratio assay kit. The present results demonstrated that FOXG1 expression was upregulated in NPC tissues and cells, and was associated with distant metastasis and TNM stage. Moreover, knockdown of FOXG1 inhibited the proliferation, migration, invasion, EMT and mitochondrial function of SUNE‑1 cells, as well as promoted cell apoptosis, while the opposite results were observed in C666‑1 cells. In conclusion, FOXG1 enhanced proliferation, migration and invasion, induced EMT and improved mitochondrial function in NPC cells. The current findings provide an adequate theoretical basis for the treatment of NPC.