inhibits the viability, proliferation, invasion, and cell cycle, and promotes apoptosis of nasopharyngeal carcinoma cells by suppressing BACH2 expression.

The aim of the present study was to explore the mechanism through which affects the viability, proliferation, migration, and invasion of nasopharyngeal carcinoma (NPC). Tissue samples were collected from the hospital department. NPC cell lines were purchased to conduct the and assays. A series of biological assays including MTT, Transwell, and wound healing assays were conducted to investigate the effects of and BACH2 on NPC cells. was down-regulated in both NPC tissues and cell lines, whereas BACH2 was up-regulated in both tissues and cell lines. overexpression inhibited NPC cell viability, proliferation, migration, and invasion but promoted cell apoptosis. The converse was true of BACH2, the down-regulation of which could inhibit the corresponding cell abilities and promote apoptosis of NPC cells. The target relationship between and BACH2 was confirmed. The epithelial-mesenchymal transition (EMT) pathway was also influenced by down-regulation. In conclusion, could bind to BACH2, inhibit NPC cell abilities, and promote cell apoptosis.