ABSTRACT

Problem and aim

The overexpression of MAP17 has been reported in various human carcinomas. However, its molecular mechanism in non-small cell lung cancer (NSCLC) has not been fully understood. Our study aimed to reveal the molecular mechanism of NSCLC that involved MAP17 and identify its target miRNA.

Methods

RT-qPCR and immunoblot assays were conducted to measure the expression of mRNA and protein in NSCLC tissues and cell lines. Meanwhile, the A549 cells (an NSCLC cell line) were randomly assigned to the MAP17 overexpression group, the MAP17 knockdown group and negative control group to study the roles of MAP17 in cell viability, cell proliferation, migration, invasion, and apoptosis by performing Trypan blue exclusion, MTT, colony formation, transwell, wound healing and flow-cytometric apoptosis assays. The luciferase reporter assay was conducted to confirm the target relationship between MAP17 and miR-27a-3p.

Results

The upregulation of MAP17 mRNA and protein was observed in NSCLC tissues and cell lines. In vitro, the positive roles of MAP17 on cell viability, migration, and invasion were confirmed in A549 cells. It was also found that MAP17 could inhibit cell apoptosis by suppressing the activation of the p38 pathway. This research eventually proved the target relationship between MAP17 and miR-27a-3p, and that miR-27a-3p reversed the effects of MAP17 in A549 cells by directly targeting MAP17.

Conclusions

MAP17 plays an oncogenic role in NSCLC by suppressing the activation of the p38 pathway. Apart from that, the miR-27a-3p can inhibit the expression of MAP17 to suppress the NSCLC progression.

中文翻译：

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MAP17通过抑制miR-27a-3p表达和p38信号通路促进非小细胞肺癌的发展

摘要

问题与目标

MAP17的过表达已在多种人类癌症中报道。但是，其在非小细胞肺癌（NSCLC）中的分子机制尚未完全了解。我们的研究旨在揭示涉及MAP17的非小细胞肺癌的分子机制，并确定其靶标miRNA。

方法

进行RT-qPCR和免疫印迹测定以测量NSCLC组织和细胞系中mRNA和蛋白质的表达。同时，将A549细胞（一种非小细胞肺癌细胞系）随机分为MAP17过表达组，MAP17敲低组和阴性对照组，以通过进行台盼盼研究MAP17在细胞活力，细胞增殖，迁移，侵袭和凋亡中的作用蓝色排斥，MTT，集落形成，穿孔，伤口愈合和流式细胞仪检测。进行荧光素酶报告基因测定以证实MAP17与miR-27a-3p之间的靶标关系。

结果

在NSCLC组织和细胞系中观察到MAP17 mRNA和蛋白的上调。在体外，在A549细胞中证实了MAP17对细胞活力，迁移和侵袭的积极作用。还发现MAP17可以通过抑制p38途径的激活来抑制细胞凋亡。这项研究最终证明了MAP17与miR-27a-3p之间的靶标关系，并且miR-27a-3p通过直接靶向MAP17逆转了A549细胞中MAP17的作用。

结论

MAP17通过抑制p38途径的激活在NSCLC中发挥致癌作用。除此之外，miR-27a-3p可以抑制MAP17的表达，从而抑制NSCLC进展。