BACKGROUND To analyze the relative expression of PELI3 and its mechanistic involvement in the non-small cell lung cancer (NSCLC). METHODS PELI3 expression in NSCLC tissue samples was determined by the immunohistochemistry. The transcripts abundance of PELI3 was measured with real-time PCR. The protein intensity was analyzed by western blot. The overall survival in respect to PELI3 or miR-365a-5p expression was plotted by the Kaplan-Meier's analysis. Cell growth was determined by colony formation assay. Cell viability was measured by MTT assay. The migration and invasion were evaluated by wound healing and transwell assay respectively. The regulatory effect of miR-365a-5p on PELI3 was interrogated with luciferase reporter assay. The direct binding between miR-365a-5p and PELI3 was analyzed by pulldown assay. RESULTS PELI3 was aberrantly up-regulated in NSCLC both in vivo and in vitro. High level of PELI3 associated with poor prognosis. PELI3-deficiency significantly inhibited cell viability, colony formation, migration and invasion. We further identified that miR-365a-5p negatively regulated PELI3 in this disease. Ectopic expression of miR-365a-5p in both A549 and H1299 phenocopied PELI3-deficiency. Meanwhile, PELI3-silencing significantly abolished the pro-tumoral effect elicited by miR-365a-5p inhibition. CONCLUSION Our results highlighted the importance of dysregulated miR-365a-5p-PELI3 signaling axis in NSCLC.

中文翻译：

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PELI3介导下调的miR-365a-5p在非小细胞肺癌中的促肿瘤作用。

背景技术分析PELI3在非小细胞肺癌（NSCLC）中的相对表达及其机制。方法采用免疫组织化学方法检测NSCLC组织中PELI3的表达。用实时PCR测量PELI3的转录本丰度。通过蛋白质印迹分析蛋白质强度。通过Kaplan-Meier分析绘制了关于PELI3或miR-365a-5p表达的总存活率。细胞生长通过集落形成测定法确定。细胞存活力通过MTT测定法测量。分别通过伤口愈合和transwell分析评估迁移和侵袭。萤光素酶报告基因检测了miR-365a-5p对PELI3的调控作用。通过下拉法分析了miR-365a-5p和PELI3之间的直接结合。结果PELI3在NSCLC体内和体外均异常上调。PELI3水平高与预后不良有关。PELI3缺乏显着抑制细胞活力，集落形成，迁移和侵袭。我们进一步发现，miR-365a-5p在这种疾病中负调控PELI3。miR-365a-5p在A549和H1299表型复制的PELI3缺陷中的异位表达。同时，PELI3沉默显着消除了miR-365a-5p抑制引起的促肿瘤作用。结论我们的结果强调了NSCLC中miR-365a-5p-PELI3信号轴失调的重要性。我们进一步发现，miR-365a-5p在这种疾病中负调控PELI3。miR-365a-5p在A549和H1299表型复制的PELI3缺陷中的异位表达。同时，PELI3沉默显着消除了miR-365a-5p抑制引起的促肿瘤作用。结论我们的结果强调了NSCLC中miR-365a-5p-PELI3信号轴失调的重要性。我们进一步发现，miR-365a-5p在这种疾病中负调控PELI3。miR-365a-5p在A549和H1299表型复制的PELI3缺陷中的异位表达。同时，PELI3沉默显着消除了miR-365a-5p抑制引起的促肿瘤作用。结论我们的结果强调了NSCLC中miR-365a-5p-PELI3信号轴失调的重要性。