Chemoresistance to cisplatin (DDP) has become a dominating obstacle to the successful treatment of nasopharyngeal carcinoma (NPC). Recently, accumulating data support the tenet that microRNAs (miRNAs) function as new crucial regulators of diverse biological processes, including chemoresistance. In this study, the miRNA expression profiles in NPC were first analyzed using miRNA microarray dataset. miR-1278 was identified as the most decreased miRNA in NPC tissues. We then validated that miR-1278 was significantly down-regulated in NPC tissues and cell lines. Moreover, decreased miR-1278 was strongly associated with worse overall survival and poor chemotherapy response. Gain-of-function experiments showed that overexpression of miR-1278 dramatically sensitized NPC cells to DDP and reduced autophagy. Mechanistically, ATG2B was identified as a target gene of miR-1278. More importantly, ATG2B overexpression reversed miR-1278-induced suppression of autophagy and DDP resistance. Taken together, our results suggested that miR-1278 inhibited the DDP resistance of NPC cells and autophagy through targeting ATG2B. miR-1278 might function as a novel therapeutic target in NPC treatment.

对顺铂的化学耐药性（DDP）已成为成功治疗鼻咽癌（NPC）的主要障碍。最近，不断积累的数据支持微RNA（miRNA）充当各种生物过程（包括化学抗性）的新关键调节因子的宗旨。在这项研究中，首先使用miRNA微阵列数据集分析了NPC中的miRNA表达谱。miR-1278被确定为NPC组织中减少最多的miRNA。然后，我们验证了miR-1278在NPC组织和细胞系中显着下调。此外，减少的miR-1278与更差的总体生存率和较差的化疗反应密切相关。功能获得性实验表明，miR-1278的过表达使NPC细胞对DDP敏感，并减少了自噬。机械上，ATG2B被鉴定为miR-1278的靶基因。更重要的是，ATG2B过表达逆转了miR-1278诱导的自噬和DDP抗性抑制。两者合计，我们的结果表明miR-1278抑制NPC细胞的DDP抵抗力并通过靶向ATG2B自噬。miR-1278可能作为NPC治疗中的新型治疗靶标。