目的  探讨miR-26a和异黏蛋白（MTDH）的关系。   方法  采用免疫组织化学SP染色法检测86例食管癌病理组织芯片中MTDH的表达，采用原位杂交检测miR-26a的表达，分析两者表达的相关性。通过生物信息学预测软件Targetscan Human7.2预测MTDH在miR-26a序列上的结合片段。采用荧光素酶报告实验验证MTDH与miR-26a的靶向调控关系。用慢病毒干扰和过表达的食管癌细胞系进行裸鼠皮下注射，观察瘤块的形成，采用免疫组织化学染色法和原位杂交法检测各组瘤体中MTDH和miR-26a的表达，分析其关系。  结果  MiR-26a在食管癌组织中的表达明显低于配对癌旁正常食管组织，而MTDH在食管癌组织中的表达明显高于配对癌旁正常食管组织。MiR-26a的表达与患者病理分级（P<0.05）、N分期（P<0.05)、肿瘤体积（P<0.01）有关。MTDH在食管癌中的表达与N分期（P<0.05）、分化程度（P<0.01）有关。采用Targetscan Human7.2生物信息学软件预测发现，MTDH基因中含有1个hsa-miR-26a的靶序列。荧光素酶报告基因实验也证实了miR-26a与MTDH的靶向调控关系。MiR-26a在KYSE-450细胞中表达最高，在Eca109细胞中表达量最低， 本研究采用KYSE-450细胞系进行miR-26a干扰实验的裸鼠实验，采用Eca109细胞系进行过表达实验。过表达miR-26a慢病毒转染的细胞注射裸鼠皮下，成瘤后miR26a的表达升高，MTDH的表达降低。干扰miR-26a慢病毒转染的细胞注射裸鼠皮下，成瘤后瘤块中miR-26a的表达降低，MTDH表达升高。   结论  MiR-26a能抑制食管癌细胞MTDH表达，在体外和体内实验，均可验证miR-26a与MTDH的靶向调控关系，miR-26a可能通过MTDH通路在食管癌的发生和发展中扮演着癌基因的角色。

Objective  To explore the relationship between miR-26a and metadherin (MTDH), and to verify the relationship between miR-26a and MTDH in vivo in nude mice.    Methods  Immunohistochemical SP staining method  was used to detect the expression of MTDH and in situ hybridization was used to detect the expression of miR-26a in 86 cases of esophageal cancer, and the correlation between the expressions was analyzed. The bioinformatics prediction Targetscan Human 7.2 software could predicte the binding fragment of MTDH on the miR-26a sequence, and the luciferase report experiment was used to verify the targeted regulatory relationship between MTDH and miR-26a. Nude mice were injected esophageal cancer cell lines subcutaneously which were lentiviral interferenced and overexpressed miR-26a to observe the formation of tumors. The tumors from nude mice were made into paraffin. and each was detected. The expression of MTDH in miR-26a in the tumor groups was detected by immunohistochemical staining and in situ hybridization and the relationship was analyzed.    Results  The expression of miR-26a in esophageal cancer tissues was significantly lower than that in paired normal esophageal tissues, and the expression of MTDH in esophageal cancer tissues was significantly higher than that in paired normal esophageal tissues. The expression of miR-26a was related to the patient’s pathological grade (P<0.05), N stage (P<0.05), and tumor volume (P<0.01). The expression of MTDH in esophageal cancer was related to the N stage (P<0.05) and the degree of differentiation (P<0.01). Targetscan Human7.2 bioinformatics software predicted that the MTDH gene contained a target sequence of hsa-miR-26a.The luciferase reporter gene experiment also verified the targeted regulation relationship between miR-26a and MTDH. The expression of miR-26a was the highest in KYSE-450 cells and the lowest in Eca109 cells. The mRNA expression of MTDH in the lv-miR-26a group was significantly lower than that in the lv-NC group, and the mRNA expression in the lv-miR-26a-inhibitor group was significantly  higher than that in the lv-NC group. After tumor formation, miR-26a expression increased and MTDH expression decreased in miR-26a group. After tumor formation, the expression of miR-26a decreased and the expression of MTDH increased in miR-26a inhibitor group.    Conclusion  MiR-26a can inhibit the expression of MTDH in esophageal cancer cells. Both in vitro and in vivo experiments can verify the targeted regulatory relationship between miR-26a and MTDH. MiR-26a may play a role in the occurrence and development of esophageal cancer through the MTDH.