星形細(xì)胞瘤為浸潤性生長腫瘤,生長緩慢,多為隱形癥狀,難以早期發(fā)現(xiàn)。多數(shù)腫瘤切除后有復(fù)發(fā)可能,且復(fù)發(fā)后腫瘤可演變成間變性星形細(xì)胞瘤或多形性膠質(zhì)母細(xì)胞瘤。因此尋找其生物標(biāo)志物早期診斷,并研究新的治療方法就十分重要。方法:通過選用GEO數(shù)據(jù)庫的星形細(xì)胞瘤miRNA表達譜數(shù)據(jù),進行差異分析以及靶基因預(yù)測,通過2者共表達網(wǎng)絡(luò)的構(gòu)建對篩選出的miRNA的研究價值進行探討。結(jié)果:得出hsa-miR-29b-2-5p;hsa-miR-339-5p與hsa-miR-362-3p3個較為關(guān)鍵的miRNA及與3者關(guān)系密切的8個mRNA。結(jié)論:通過對8個mRNA在癌癥中的作用的討論,肯定了這3個關(guān)鍵miRNA作為潛在靶點的研究價值。 

【文章來源】：生物信息學(xué). 2020,18(04)

【文章頁數(shù)】：7 頁

【部分圖文】：

GSE138764數(shù)據(jù)集中篩選后的各5個上調(diào)和下調(diào)的差異miRNA熱圖

表 2 通過miRBD與Starbase v2.0預(yù)測與驗證的差異miRNA的靶基因Table 2 Target genes of differential miRNAs predicted and verified by miRBD and Starbase v2.0 miRNAID Tatget gene miRNAID Target gene hsa-miR-29b-2-5p POU2F2 hsa-miR-505-3p HMGB1 hsa-miR-29b-2-5p WNK1 hsa-miR-505-3p DHX15 hsa-miR-29b-2-5p LRRTM2 hsa-miR-505-3p VGLL3 hsa-miR-29b-2-5p TTC17 hsa-miR-505-3p GLYR1 hsa-miR-29b-2-5p ZFHX3 hsa-miR-505-3p RBMS3 hsa-miR-29b-2-5p GUCY1A2 hsa-miR-505-3p SCLT1 hsa-miR-29b-2-5p EIF5B hsa-miR-505-3p LRRCC1 hsa-miR-29b-2-5p SGIP1 hsa-miR-505-3p SNX30 hsa-miR-29b-2-5p FAM160B1 hsa-miR-505-3p CREBRF hsa-miR-29b-2-5p MAK16 hsa-miR-505-3p PTBP2 hsa-miR-377-5p TMEM30B hsa-miR-339-5p MAPRE1 hsa-miR-377-5p AGO1 hsa-miR-339-5p BACE1 hsa-miR-377-5p ZFP82 hsa-miR-339-5p FAM219B hsa-miR-377-5p TFPI hsa-miR-339-5p WDR81 hsa-miR-377-5p DDA1 hsa-miR-339-5p NXPH1 hsa-miR-377-5p EIF5A2 hsa-miR-339-5p SLC15A2 hsa-miR-377-5p BATF2 hsa-miR-339-5p KMT2A hsa-miR-377-5p PRRC1 hsa-miR-339-5p SORT1 hsa-miR-377-5p MSL2 hsa-miR-339-5p DIPK2A hsa-miR-377-5p TRIO hsa-miR-339-5p C2orf83 hsa-miR-431-3p WDR48 hsa-miR-424-5p PAPPA hsa-miR-431-3p P2RY13 hsa-miR-424-5p FASN hsa-miR-431-3p ITGA11 hsa-miR-424-5p UNC80 hsa-miR-431-3p JAZF1 hsa-miR-424-5p FGF2 hsa-miR-431-3p C15orf62 hsa-miR-424-5p TNRC6B hsa-miR-431-3p PDE7A hsa-miR-424-5p PTPN4 hsa-miR-431-3p COPS9 hsa-miR-424-5p PHF19 hsa-miR-431-3p RBPMS hsa-miR-424-5p UBE2Q1 hsa-miR-431-3p DRAXIN hsa-miR-424-5p LSM11 hsa-miR-431-3p MTRNR2L3 hsa-miR-424-5p ANKUB1 hsa-miR-770-5p GMFB hsa-miR-362-3p PPP2R2D hsa-miR-770-5p MAP3K1 hsa-miR-362-3p PTBP2 hsa-miR-770-5p SLC17A6 hsa-miR-362-3p BLCAP hsa-miR-770-5p CCND2 hsa-miR-362-3p TNRC6B hsa-miR-770-5p MARK1 hsa-miR-362-3p TENT4B hsa-miR-770-5p DSE hsa-miR-362-3p DLGAP4 hsa-miR-770-5p ARHGAP12 hsa-miR-362-3p SMNDC1 hsa-miR-770-5p UBR3 hsa-miR-362-3p SRSF4 hsa-miR-770-5p PPP3CA hsa-miR-362-3p SHB hsa-miR-770-5p TDP1 hsa-miR-362-3p KLHL2 hsa-miR-485-5p KCNB1 hsa-miR-181a-2-3p FLI1 hsa-miR-485-5p PLXNA4 hsa-miR-181a-2-3p SORBS1 hsa-miR-485-5p PHTF2 hsa-miR-181a-2-3p BLOC1S5 hsa-miR-485-5p GPN3 hsa-miR-181a-2-3p PELI2 hsa-miR-485-5p SLC36A3 hsa-miR-181a-2-3p ARID4A hsa-miR-485-5p MSI2 hsa-miR-181a-2-3p DAZL hsa-miR-485-5p OGT hsa-miR-181a-2-3p ACVR2B hsa-miR-485-5p ADAMTSL5 hsa-miR-181a-2-3p SOX6 hsa-miR-485-5p ZBTB39 hsa-miR-181a-2-3p NETO2 hsa-miR-485-5p CKS1B hsa-miR-181a-2-3p RNF135與hsa-miR-29b-2-5p關(guān)系密切的關(guān)鍵mRNA為POU2F2與CCND2。在轉(zhuǎn)移性GC細(xì)胞系和患者樣品中檢測到POU2F2表達增加。 POU2F2是由核因子(NF)-κB的激活誘導(dǎo)的,進而調(diào)節(jié)ROBO1轉(zhuǎn)錄,因此在功能上有助于GC轉(zhuǎn)移。研究表明,NF-κB和以POU2F2為中心的SLIT2 / ROBO1相互作用網(wǎng)絡(luò)可能對腫瘤轉(zhuǎn)移起關(guān)鍵作用,miR-218為已知的能夠調(diào)控POU2F2的miRNA,前體阻斷面向POU2F2的轉(zhuǎn)移網(wǎng)絡(luò)的激活[11]。細(xì)胞周期蛋白D2(CCND2)是D型細(xì)胞周期蛋白的成員,在細(xì)胞周期調(diào)節(jié),分化和惡性轉(zhuǎn)化中起著關(guān)鍵作用。有研究表明明CCND2表達的降低與啟動子異常甲基化密切相關(guān)[12]。


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