Jiang Wenhua, Zheng Liangda, Yan Qingqing, Chen Lili, Wang Xianting
Department of Hematology and Oncology, Taizhou First People's Hospital, Taizhou 318020, China.
J BUON. 2019 Nov-Dec;24(6):2287-2293.
To investigate the potential effect of microRNA-532-5p (miR-532-3p) on the development of non-small cell lung cancer (NSCLC) and the relevant mechanism.
Thirty-seven patients who underwent primary NSCLC resection were studied. To examine the role of miR-532-3p in NSCLC development, we detected the level of miR-532-3p expression in NSCLC tissues and the para-cancer tissues by qRT-PCR. In order to investigate the potential target of miR-532-3p, we checked it in three publicly available algorithms, TargetScan, miRDB and microRNA, to elucidate the putative and possible targets of miR-532-3p. To test the function of miR-532-3p on the proliferation of NSCLC cell, we performed MTT assay to detect the cell proliferation rates. Migration and invasion were also studied.
The expression level of miR-532-3p were detected in NSCLC tissues and cells by qRT-PCR, which indicated that the expression of miR-532-3p was low in both tissue and cell levels. Online prediction websites and luciferase reporter assay indicated that FOXP3 is a direct target of miR-532-3p in NSCLC cells. Further results showed that this miR significantly decreased the expression level of FOXP3. MTT assay showed that miR-532-3D remarkably suppressed the proliferation of NSCLC cells. Furthermore, transwell and scratch healing experiments suggested that miR-532-3p inhibited the invasion and migration of NSCLC cells.
Our research discovered the suppressive function of miR-532-3p in NSCLC by targeting FOXP3, revealing that miR-532-3p/FOXP3 axis might be a potential therapeutic target for the treatment of NSCLC.
探讨微小RNA-532-5p(miR-532-3p)对非小细胞肺癌(NSCLC)发生发展的潜在影响及其相关机制。
对37例行原发性NSCLC切除术的患者进行研究。为检测miR-532-3p在NSCLC发生发展中的作用,我们采用qRT-PCR检测NSCLC组织及癌旁组织中miR-532-3p的表达水平。为研究miR-532-3p的潜在靶标,我们在三个公开可用的算法TargetScan、miRDB和microRNA中进行了检查,以阐明miR-532-3p的假定和可能靶标。为测试miR-532-3p对NSCLC细胞增殖的作用,我们进行MTT试验以检测细胞增殖率。还研究了迁移和侵袭情况。
通过qRT-PCR检测NSCLC组织和细胞中miR-532-3p的表达水平,结果表明miR-532-3p在组织和细胞水平上的表达均较低。在线预测网站和荧光素酶报告基因试验表明,FOXP3是NSCLC细胞中miR-532-3p的直接靶标。进一步结果显示,该miR显著降低了FOXP3的表达水平。MTT试验表明,miR-532-3D显著抑制了NSCLC细胞的增殖。此外,Transwell和划痕愈合实验表明,miR-532-3p抑制了NSCLC细胞的侵袭和迁移。
我们的研究发现miR-532-3p通过靶向FOXP3对NSCLC具有抑制作用,揭示miR-532-3p/FOXP3轴可能是NSCLC治疗的潜在靶点。