miR-138在鼻咽癌患者中的预后价值及其对细胞增殖、迁移和侵袭的影响

Prognostic Value of miR-138 in Nasopharyngeal Carcinoma and its Effects on Cell Proliferation,Migration,and Invasion

目的探讨miR-138在鼻咽癌中的临床意义以及对癌细胞增殖、迁移和侵袭的影响。方法采用实时荧光定量PCR检测鼻咽癌组织和癌细胞CNE1中miR-138的表达量。采用Kaplan-Meier生存分析和Cox回归分析评估miR-138的预后价值。构建体外调控miR-138表达量的鼻咽癌细胞体系,采用MTT法和Transwell实验法分析miR-138对癌细胞CNE1生命活动的影响。结果 miR-138在鼻咽癌组织和细胞中的表达量均显著下调(P<0.001),且与癌症患者的淋巴结转移(P=0.007)及TNM分期(P=0.003)密切相关。生存曲线表明,低表达miR-138的鼻咽癌患者较高表达患者具有较差的总生存率(P=0.002),且可以作为一个独立的预后因子(HR=2.603,95%CI=1.245~5.441,P=0.011)应用在鼻咽癌的治疗中。体外细胞实验证明,高表达miR-138具有抑制鼻咽癌细胞CNE1增殖、迁移和侵袭的能力(P<0.05),而抑制miR-138的表达则显著促进癌细胞的各种生命活动(P<0.05)。结论 miR-138与鼻咽癌的预后密切相关,且可以明显抑制鼻咽癌细胞CNE1的增殖、迁移和侵袭能力。

Objective The purpose of this study was to investigate the clinical significance of miR-138 and its effects on proliferation,migration,and invasion in nasopharyngeal carcinoma（NPC）cell. Methods Quantitative real-time polymerase chain reaction（qRT-PCR）was used to estimate the expression levels of miR-138 in NPC tissues and CNE1 cells. The prognostic value of miR-138 was evaluated using Kaplan-Meier methods and Cox regression analysis. MTT and Transwell analyses were adopted to examine the cell proliferation,migration,and invasion in CNE1 cells. Results Downregulated expression of miR-138 was detected in both NPC tissues and cells（all P〈0.001）,and correlated with lymph node metastasis（P=0.007）and TNM stage（P=0.003）. According to the survival curves,patients with low miR-138 expression had poor overall survival than those with high miR-138 expression（Log-rank P=0.002）. The results of Cox analysis showed that miR-138（HR=2.603,95%CI=1.245～5.441,P=0.011）was an independent prognostic factor for NPC patients. The data of cell experiments revealed that overexpression of miR-138 could suppress CNE1 cell proliferation,migration and invasion（all P〈0.05）,while the knockdown of miR-138 could promote the CNE1 cell proliferation,migration,and invasion（all P〈0.05）. Conclusion miR-138 expression is closely associated with prognosis of NPC and can suppress the proliferation,metastasis,and invasion of CNE1 cells.