摘要目的 探讨长链非编码RNA(lncRNA) RP11-316M1.12在乳腺癌中的作用及相关机制.方法 生物信息学统计RP11-316M1.12在乳腺癌组织及正常组织中的表达量,qRT-PCR方法检测RP11-316M1.12在乳腺癌组织及乳腺癌细胞中的表达量,统计分析RP11-316M1.12的表达量与乳腺癌临床特征的关系.在MCF-7细胞中过表达RP11-316M1.12,在MDA-MB-231细胞中敲低RP11-316M1.12,Transwell方法检测上述细胞的侵袭能力,Western blot技术检测上述细胞上皮间质转化(EMT)标志物的表达.结果 GEPIA数据库资料显示RP11-316M1.12在乳腺癌组织中表达量显著高于正常组织.qRT-PCR检测在65例乳腺癌组织和23例癌旁组织中得到相似的结果,且发现RP11-316M1.12在乳腺癌细胞中的表达量高于乳腺正常上皮细胞.RP11-316M1.12表达与乳腺癌TNM分期及远处转移有关.Transwell结果显示过表达RP11-316M1.12可促进MCF-7细胞的侵袭能力,而敲低RP11-316M1.12可显著抑制MDA-MB-231细胞的侵袭能力.机制研究发现过表达RP11-316M1.12可下调E-cadhefin,同时上调Vimentin和ZEB1.结论 RP11-316M1.12在乳腺癌中高表达且增强乳腺癌细胞侵袭能力.

abstractsObjective To explore the role and mechanism of long non-coding RNA (lncRNA)RP11-316M1.12 in breast cancer cells.Methods Bioinformatics analysis was performed to varify RP11-316M1.12 expression pattern in breast cancer tissues and normal tissues.Quantitative real time polymerase chain reaction (qRT-PCR) assay was used to check the expression level of RP11-316M1.12 in breast cancer cells and tissues.Further,the correlationship between RP11-316M1.12 expression and clinical paremeters of breast cancer was analysed according to RP11-316M1.12 level.RP11-316M1.12 was overexpressed in MCF-7 cells,and RP11-316M1.12 was knocked down in MDA-MB-231 cells.Transwell method was used to detect the invasive ability of these cells.Western blot was used to detect the expression of epithelialmesenchymal transition (EMT) markers in these cells.Results Gene Expression Profiling Interactive Analysis (GEPIA) database suggested that RP11-316M1.12 was highly expressed in breast cancer tissues than that in normal tissues.The similar results were got in 65 cases of breast cancer tissues and 23 cases of normal tissues by qRT-PCR assay.Meanwhile,we found that RP11-316M1.12 was enhanced in breast cancer cells than that in normal epithelial cell and RP11-316M1.12 expression is related to TNM stage and distant metastasis in breast cancer.Transwell assay demonstrated that RP11-316M1.12 significantly enhanced breast cancer cells invasion.Mechanismly,over expression of RP11-316M1.12 can remakably downregulated E-cadherin,enhanced ZEB1 and Vimentin expression in these cells.Conclusions RP11-316M1.12 was enhanced in breast cancer,and RP1 1-316M1.12 could accelerate invasion of breast cancer cells.