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微小RNA-532-3p通过靶向叉头框蛋白P3抑制非小细胞肺癌的转移和增殖。

MiR-532-3p inhibits metastasis and proliferation of non-small cell lung cancer by targeting FOXP3.

作者信息

Jiang Wenhua, Zheng Liangda, Yan Qingqing, Chen Lili, Wang Xianting

机构信息

Department of Hematology and Oncology, Taizhou First People's Hospital, Taizhou 318020, China.

出版信息

J BUON. 2019 Nov-Dec;24(6):2287-2293.

Abstract

PURPOSE

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.

METHODS

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.

RESULTS

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.

CONCLUSIONS

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.

摘要

目的

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。

方法

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。

结果

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。

结论

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。

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