The rs619586 polymorphism has been shown to alter the expression of MALAT1, which act as a competing endogenous RNA (ceRNA) against miR‐145. And miR‐145 was found to target COL5A1, the interaction between which was shown to be involved in the pathogenesis of invasive meningioma. In this study, we aimed to explore the effect of rs619586 polymorphism and its underlying molecular mechanism in invasive meningioma. Real‐time PCR and Western Blot analysis were used to study the differentiated expression of miR‐145, MALAT1 (metastasis‐associated lung adenocarcinoma transcript 1) and COL5A1 (collagen alpha‐1(V) chain) in tumour/serum samples genotyped as rs619586 AA, AG and GG. Computational analysis and luciferase reporter assay were also conducted to identify the regulatory relationship between miR‐145 and MALAT1/COL5A1. Meanwhile, expression of miR‐145 and COL5A1 in different cell treatment groups was measured to validate the results obtained from earlier experiments. As shown by the results and in tumour/serum samples genotyped as AA, AG and GG, the expression of both MALAT1 and COL5A1 was down‐regulated in a stepwise fashion, while the expression of miR‐145 was increased, suggesting a potential negative relationship between MALAT1/COL5A1 and miR‐145. Meanwhile, miR‐145 was shown to bind to MALAT1, while COL5A1 was identified as a virtual target gene of miR‐145. As a consequence, a MALAT1/miR‐145/COL5A1 molecular pathway was established based on the above results. In particular, with the presence of rs619586 A>G polymorphism, the expression of MALAT1 and COL5A1 was both reduced, leading to reduced invasiveness of meningioma.

中文翻译：

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MALAT1中的rs619586多态性等位基因通过调节V型胶原（COL5A1）的表达来改变脑膜瘤的侵袭性。

rs619586基因多态性已显示可改变MALAT1的表达，MALAT1可作为对抗miR-145的竞争性内源RNA（ceRNA）。发现miR‐145靶向COL5A1，两者之间的相互作用被证明与浸润性脑膜瘤的发病机制有关。在这项研究中，我们旨在探讨rs619586基因多态性及其在侵袭性脑膜瘤中的分子机制的作用。实时PCR和Western Blot分析用于研究基因型为rs619586的肿瘤/血清样本中miR‐145，MALAT1（与转移相关的肺腺癌转录本1）和COL5A1（胶原α-1（V）链）的差异表达。 AA，AG和GG。还进行了计算分析和荧光素酶报告基因分析，以确定miR-145和MALAT1 / COL5A1之间的调节关系。与此同时，测量不同细胞处理组中miR‐145和COL5A1的表达，以验证从早期实验中获得的结果。结果表明，在基因型为AA，AG和GG的肿瘤/血清样本中，MALAT1和COL5A1的表达均呈逐步下调的趋势，而miR-145的表达则呈上升趋势，表明存在潜在的负相关在MALAT1 / COL5A1和miR‐145之间。同时，显示miR-145与MALAT1结合，而COL5A1被鉴定为miR-145的虚拟靶基因。因此，基于上述结果建立了MALAT1 / miR-145 / COL5A1分子途径。特别地，由于存在rs619586A> G多态性，MALAT1和COL5A1的表达均降低，导致脑膜瘤的浸润性降低。