The aim of the present study was to explore the mechanism through which miR-130a-3p 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 in vitro and in vivo assays. A series of biological assays including MTT, Transwell, and wound healing assays were conducted to investigate the effects of miR-130a-3p and BACH2 on NPC cells. MiR-130a-3p was down-regulated in both NPC tissues and cell lines, whereas BACH2 was up-regulated in both tissues and cell lines. MiR-130a-3p 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 miR-130a-3p and BACH2 was confirmed. The epithelial–mesenchymal transition (EMT) pathway was also influenced by miR-130a-3p down-regulation. In conclusion, miR-130a-3p could bind to BACH2, inhibit NPC cell abilities, and promote cell apoptosis.
Three months to 5 years follow-up of 21 patients were accomplished by pure tone audiometry and other details. There was no recurrent cholesteatoma in the patients. Compared with pre-operative average bone conduction at 0.5, 1, 2, 4, and 8 kHz, 12 cases had a difference less than 5 dB, three patients' hearing improved (more than 10 dB), and five cases declined (more than 10 dB). One patient received cochlear implantation 3 months after the surgery. The average bone and air conduction thresholds at 0.5, 1, 2, 4, and 8 kHz had no obvious change (p > 0.05) in 11 patients managed by a canal wall down mastoidectomy with tympanoplasty.
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