Ryu Dongchan, Lee Chaeyoung
Department of Bioinformatics and Life Science, Soongsil University, Dongjak-gu, Seoul, Korea.
Medicine (Baltimore). 2017 Jan;96(1):e5817. doi: 10.1097/MD.0000000000005817.
A genome-wide association study (GWAS) was conducted to identify expression quantitative trait loci (eQTLs) for the genes involved in phosphatidylinositol-3-kinase/v-akt murine thymoma viral oncogene homolog (PI3K/AKT) pathway.Data on mRNA expression of 341 genes in lymphoblastoid cell lines of 373 Europeans recruited by the 1000 Genomes Project using Illumina HiSeq2000 were utilized. We used their genotypes at 5,941,815 nucleotide variants obtained by Genome Analyzer II and SOLiD.The association analysis revealed 4166 nucleotide variants associated with expression of 85 genes (P < 5 × 10). A total of 73 eQTLs were identified as association signals for the expression of multiple genes. They included 9 eQTLs for both of the genes encoding collagen type I alpha 1 (COL1A1) and integrin alpha 11 (ITGA11), which synthesize a major complex of plasma membrane. They also included eQTLs for type IV collagen molecules; 13 eQTLs for both collagen type IV alpha 1 (COL4A1) and collagen type IV alpha 2 (COL4A2) and 18 eQTLs for both collagen type IV alpha 5 (COL4A5) and collagen type IV alpha 6 (COL4A6). Some genes expressed by the eQTLs might induce expression of the genes encoding type IV collagen. One eQTL (rs16871986) was located in the promoter of palladin (PALLD) gene which might synthesize collagen by activating fibroblasts through the PI3K/AKT pathway. Another eQTL (rs34845474) was located in an enhancer of cadherin related family member 3 (CDHR3) gene which can mediate cell adhesion.This study showed a profile of eQTLs for the genes involved in the PI3K/AKT pathway using a healthy population, revealing 73 eQTLs associated with expression of multiple genes. They might be candidates of common variants in predicting genetic susceptibility to cancer and in targeting cancer therapy. Further studies are required to examine their underlying mechanisms for regulating expression of the genes.
开展了一项全基因组关联研究(GWAS),以鉴定参与磷脂酰肌醇-3-激酶/v-akt鼠科胸腺瘤病毒癌基因同源物(PI3K/AKT)通路的基因的表达数量性状位点(eQTL)。利用了千人基因组计划通过Illumina HiSeq2000招募的373名欧洲人的淋巴母细胞系中341个基因的mRNA表达数据。我们使用了他们在通过基因组分析仪II和SOLiD获得的5,941,815个核苷酸变异位点的基因型。关联分析揭示了4166个与85个基因的表达相关的核苷酸变异位点(P<5×10)。总共鉴定出73个eQTL作为多个基因表达的关联信号。其中包括编码I型胶原α1(COL1A1)和整合素α11(ITGA11)的两个基因的9个eQTL,它们合成质膜的主要复合物。还包括IV型胶原分子的eQTL;IV型胶原α1(COL4A1)和IV型胶原α2(COL4A2)的13个eQTL以及IV型胶原α5(COL4A5)和IV型胶原α6(COL4A6)的18个eQTL。由eQTL表达的一些基因可能会诱导IV型胶原编码基因的表达。一个eQTL(rs16871986)位于帕拉丁(PALLD)基因的启动子中,该基因可能通过PI3K/AKT通路激活成纤维细胞来合成胶原。另一个eQTL(rs34845474)位于钙黏蛋白相关家族成员3(CDHR3)基因的增强子中,该基因可介导细胞黏附。本研究展示了使用健康人群对参与PI3K/AKT通路的基因的eQTL概况,揭示了73个与多个基因表达相关的eQTL。它们可能是预测癌症遗传易感性和靶向癌症治疗的常见变异的候选者。需要进一步研究来检查它们调节基因表达的潜在机制。