MARVELD1调控内含子miR-186、miR-335表达的研究

目的:前期研究发现,MARVELD1(具有囊泡运输和膜连接功能的MAL及相关蛋白1)在多种肿瘤细胞中表达下调,许多micro RNAs也随其发生变化。本研究探讨了MARVELD1调控mi R-186和mi R-335的表达方式。方法:本研究选取了多种肺癌细胞系,运用q RT-PCR的方法检测了MARVELD1以及mi R-186和mi R-335的表达情况,通过MARVELD1过表达体系和si RNA干扰MARVELD1表达的体系分析mi R-186和mi R-335表达变化情况,运用生物信息学网站对mi R-186和mi R-335进行分析,确认其是否为内含子mi RNA,并进一步应用MARVELD1过表达和RNAi体系检测MARVELD1对mi R-186和mi R-335的宿主基因的影响。结果:在肺癌细胞中,MARVELD1与mi R-186、mi R-335的表达呈现明显的正相关。在过表达MARVELD1之后,mi R-186、mi R-335出现高表达;当下调MARVELD1表达时,mi R-186、mi R-335则表现低表达。生物信息学分析发现mi R-186和mi R-335均为内含子mi RNA。进一步分析MARVELD1与mi R-186和mi R-335宿主基因的表达关系显示,MARVELD1可以上调它们的宿主基因的表达。结论:上述结果表明,MARVELD1可通过影响内含子mi R-186和mi R-335的宿主基因进而调控二者的表达,为进一步研究MARVELD1影响肿瘤细胞的发生机制奠定了基础。

A Research of Intronic miR-186 and miR-335 Regulated byMARVELD1

Objective:It was reported that MARVELD1 downregulated in a variety of tumor cells, but also with its many microRNAs changes. This study investigated the expression of miR-186 and miR-335 which is regulated by MARVELD1.Methods:First, a variety of lung cancer cell lines were selected for the study, using qRT-PCR method to detect the expression of MARVELD1, miR-186 and miR-335. Then, the changes of miR-186 and miR-335 expression by MARVELD1 overexpression and MARVELD1 low-expression were analyzed to confirm whether there were intronic miRNA through bioinformatic analysis of miR-186 and miR-335, and MARVELD1 effects on host genes of miR-186 and miR-335 were detected by using system of MARVELD1 overexpression and MARVELD1 RNAi.Results:The expression of miR-186 and miR-335 showed a significant positive correlation with MARVELD1 in lung cancer cells. When overexpressed MARVELD1, miR-186 and miR-335 showed high expression; conversely downregulated MARVELD1, the expression of miR-186 and miR-335 decreased. Bioinformatics analysis found that miR-186 and miR-335 are intronic microRNAs. MARVELD1 can upregulate host genes expression of miR-186 or miR-335.Conclusion:These results indicate that MARVELD1 regulated the expression of intronic miR-186 and miR-335 by regulating their host genes. Our study laid the basis for further clarification of the mechanismof MARVELD1 affecting tumor cells.