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ANLN 受 miR-30a-5p 调控,介导肺腺癌的恶性进展。

ANLN Regulated by miR-30a-5p Mediates Malignant Progression of Lung Adenocarcinoma.

机构信息

Department of Thoracic Surgery, Jiangyin Hospital of Traditional Chinese Medicine, Jiangyin Hospital Affiliated to Nanjing University of Chinese Medicine, Jiangyin 214400, China.

出版信息

Comput Math Methods Med. 2021 Nov 5;2021:9549287. doi: 10.1155/2021/9549287. eCollection 2021.

Abstract

BACKGROUND

ANLN and miR-30a-5p may be involved in the progression of lung adenocarcinoma (LUAD). However, their underlying mechanism in LUAD has not been completely comprehended.

METHODS

Differential expression analysis, binding site prediction, and survival analysis were conducted by bioinformatics approaches. ANLN mRNA and miR-30a-5p expression were detected by qRT-PCR. ANLN protein expression was detected by western blot. Cell behaviors in LUAD were examined by functional experiments.

RESULTS

ANLN was activated in LUAD cells in terms of mRNA and protein. High ANLN level was positively correlated with poor prognosis. Enforced ANLN stimulated protumorigenesis LUAD cell behaviors. miR-30a-5p could target ANLN mRNA, as revealed and verified through assays. Remarkably low miR-30a-5p expression was observed in LUAD cells, and it could repress ANLN expression. The accelerated cell behaviors by overexpression of ANLN were counteracted by upregulating miR-30a-5p.

CONCLUSION

Overall, miR-30a-5p remarkably restrained the malignant progression of LUAD cells by constraining ANLN expression. Thus, ANLN and miR-30a-5p could be novel therapeutic targets of LUAD.

摘要

背景

卷曲螺旋结构域蛋白 22(ANLN)和 miR-30a-5p 可能参与肺腺癌(LUAD)的进展。然而,其在 LUAD 中的潜在机制尚未完全阐明。

方法

通过生物信息学方法进行差异表达分析、结合位点预测和生存分析。采用 qRT-PCR 检测 ANLN mRNA 和 miR-30a-5p 的表达。采用 Western blot 检测 ANLN 蛋白表达。通过功能实验检测 LUAD 中的细胞行为。

结果

在 LUAD 细胞中,ANLN 在 mRNA 和蛋白水平上均被激活。高 ANLN 水平与不良预后呈正相关。过表达 ANLN 可刺激促肿瘤发生的 LUAD 细胞行为。miR-30a-5p 可以靶向 ANLN mRNA,通过实验证实和验证。在 LUAD 细胞中观察到 miR-30a-5p 表达显著降低,可抑制 ANLN 表达。过表达 ANLN 加速的细胞行为可通过上调 miR-30a-5p 得到抑制。

结论

总体而言,miR-30a-5p 通过抑制 ANLN 表达显著抑制 LUAD 细胞的恶性进展。因此,ANLN 和 miR-30a-5p 可能成为 LUAD 的新治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eae3/8589480/d92226c552a1/CMMM2021-9549287.001.jpg

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