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进展

摘要

问题与目标

MAP17 的过度表达已在各种人类癌症中有所报道。然而，其在非小细胞肺癌（NSCLC）中的分子机制尚未完全清楚。我们的研究旨在揭示涉及 MAP17 的 NSCLC 的分子机制并确定其目标 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（NSCLC 细胞系）随机分配到 MAP17 过表达组、MAP17 敲低组和阴性对照组，通过台盼法研究 MAP17 在细胞活力、细胞增殖、迁移、侵袭和凋亡中的作用。蓝色排除、MTT、集落形成、transwell、伤口愈合和流式细胞术凋亡测定。进行荧光素酶报告基因检测以确认 MAP17 和 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，MAP17 对细胞活力、迁移和侵袭的积极作用在 A549 细胞中得到证实。还发现MAP17可以通过抑制p38通路的激活来抑制细胞凋亡。本研究最终证明了MAP17与miR-27a-3p的靶点关系，miR-27a-3p通过直接靶向MAP17逆转了MAP17在A549细胞中的作用。

结论

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