Clin Chem:miRNA-3162-5p介导的Kallikrein家族成员间的交谈

2019-08-03 不详 MedSci原创

众所周知,<span lang="EN-US" style="font-size:12.0pt;mso-bidi-font-size:14.0pt;font-family:&quot;Calibri&quot;,&quot;sans-serif&quot;; mso-fareast-font-family:宋体;mso-bidi-font-family:&quot;Times New Roman

众所周知,MicroRNAs通过优先结合到靶基因的3 ' untranslation region (3 ' UTR)抑制靶基因表达。研究表明,它们通过单核苷酸多态性(SNPs),即miRSNPs与前列腺癌(PCa)风险相关。在一个欧洲队列研究中,已经确定了22PCa风险相关的mirsnpkallikrein相关肽酶3 (KLK3) 3UTR中最显著的miRSNPmiR-3162-5p创造了一个结合位点。在此,研究人员探讨了miR-3162-5p - klk相互作用以及miR-3162-5pPCa中的临床意义。

研究人员使用核细胞活细胞成像和非锚定生长试验测试miR-3162-5p在前列腺癌病因学中的作用。同时,采用RT-quantitative (q)PCRtarget pulldown检测miR-3162-5pKLK和雄激素受体(AR)表达的影响。由DELFIA®免疫分析法测定KLK3蛋白水解活性。并通过质谱鉴定了miR-3162-5p影响的通路,采用RT-qPCR检测miR-3162-5p临床标本中的表达。

研究显示,miR-3162-5p通过直接靶向调控KLK2-4AR的表达,影响LNCaP细胞的增殖、迁移和集落形成。miR-3162-5p调控KLK3蛋白表达,lncap条件培养基中KLK3蛋白水解活性较低。KLK/Arpull-dowm和质谱分析显示miR-3162-5p在通过KLK/AR和其他靶点的代谢通路中可能发挥作用。在Gleason分级较高的前列腺肿瘤组织中,miR-3162-5p表达增加。

我们的研究通过靶向KLKsAR,深入了解miR-3162-5p可能参与前列腺癌的病因学,同时也强了调miR-3162-5p及其相互作用分子作为一类新的前列腺癌生物标志物和治疗靶点的临床应用。

原始出处:

Farhana Matin, Varinder Jeet,MicroRNA-3162-5p-Mediated Crosstalk between Kallikrein Family Members Including Prostate-Specific Antigen in Prostate Cancer

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    2020-04-01 smallant2002
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    2019-08-05 Homburg
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    2019-08-05 膀胱癌