【摘要】 目的:探讨LETM2在食管鳞癌(esophageal squamous cell carcinoma,ESCC)中的表达,研究LETM2对ESCC细胞系KYSE150和ECA109增殖和侵袭迁移的影响。方法:免疫组化(immunohistochemistry,IHC)检测90例ESCC及癌旁组织LETM2蛋白表达差异,RT-PCR和Western blot检测ESCC细胞系LETM2表达情况,慢病毒敲低KYSE150和ECA109细胞中LETM2表达。MTT和克隆形成技术检测LETM2对ESCC细胞增殖和克隆形成能力的影响,流式细胞术检测细胞周期变化,Transwell法分析LETM2敲低后细胞迁移侵袭能力的差异。结果:在ESCC组织中LETM2的表达显著高于癌旁组织,LETM2通过抑制ESCC细胞G1期向S期转化进而抑制细胞增殖,但对侵袭和迁移能力影响不大。结论:LETM2可能作为驱动基因促进ESCC的发生发展,是ESCC的关键遗传变异,可能作为ESCC早诊早治的分子标志物。更多还原

【Abstract】 Objective: To analyze the expression of LETM2 in KYSE150 and ECA109 cell lines and its effect on the proliferation, migration, and invasion of esophageal squamous cell carcinoma(ESCC). Methods: The expression level of the LETM2 protein in 90 paired human ESCC tissues and matched adjacent normal tissues was determined through immunohistochemistry. The expression level of LETM2 in ESCC cell lines was detected by real-time PCR and Western blot. The expression levels of LETM2 in KYSE150 and ECA109 cell lines were knocked down using lentivirus. MTT assays were performed to examine the effect of LETM2 on the proliferation of ESCC cells. Colony formation assay was used to detect the colony formation ability. Flow cytometry was performed to analyze the cell cycle.The effect of LETM2 depletion on the migration and invasion of ESCC cells was determined by Transwell assay. Results: LETM2 expression was frequently upregulated in the ESCC tissues than in the adjacent normal tissues. The suppressed exogenous expression of LETM2 led to the inhibition of cell proliferation and colony formation. However, cell migration and invasion were not affected. The results on the cell cycle distribution revealed that LETM2 knockdown acts as a negative regulator of the cell cycle at the G1 to S phase transition. Conclusion: LETM2 acts as a tumor-driven gene in the development and progression of ESCC. This finding suggests that LETM2 can be used as an efficient prognosis biomarker and a potential therapeutic target for ESCC.更多还原