miR-31-5p modulates cell progression in lung adenocarcinoma through TNS1/p53 axis

被引:23
作者
Zhu, Chaonan [1 ]
Wang, Shuai [2 ]
Zheng, Maogen [2 ]
Chen, Zhiquan [2 ]
Wang, Guochen [2 ]
Ma, Jun [3 ]
Zhang, Bin [1 ]
Huang, Wuhao [1 ]
Sun, Xiaoyan [1 ]
Wang, Changli [1 ]
机构
[1] Tianjin Med Univ, Key Lab Canc Prevent & Therapy, Tianjin Lung Canc Ctr,Natl Clin Res Ctr Canc, Tianjins Clin Res Ctr Canc,Dept Lung Canc,Canc In, Tianjin 300060, Peoples R China
[2] North China Univ Sci & Technol, Dept Thorac Surg, Affiliated Hosp, Tangshan 063000, Peoples R China
[3] Shanxi Prov Peoples Hosp, Dept Thorac Surg, Taiyuan 030012, Peoples R China
关键词
Proliferation; Migration; Apoptosis; Lung cancer; miRNA; CANCER; MANAGEMENT; MICRORNAS;
D O I
10.1007/s00066-021-01895-x
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Objective To clarify the modulatory mechanism of miR-31-5p in lung adenocarcinoma (LUAD) progression in vivo and in vitro. Methods The Cancer Genome Atlas (TCGA) database was employed to access LUAD-related miRNA and mRNA expression data. Downstream targets of miR-31-5p were predicted by public databases. The interaction between miR-31-5p and TNS1 was determined by dual-luciferase reporter assay. Quantitative real-time polymerase chain reaction (qRT-PCR) was utilized to measure miR-31-5p and TNS1 expression levels in LUAD cells. Western blot was introduced to test protein expression levels of TNS1, p53, and apoptosis-related proteins. In-vitro functional assays were conducted to evaluate the biological effects of miR-31-5p on cell proliferation, colony formation, migration, and apoptosis. In-vivo tumor xenograft experiment was applied to examine the effects of miR-31-5p on LUAD tumor growth, followed by immunochemistry assays for assessing TNS1 and p53 expression levels in the tumor tissue. Results miR-31-5p was prominently upregulated in LUAD tissue and was identified to present a similar trend in LUAD cell lines H1299, H23, and A549. miR-31-5p overexpression exerted an active role in cell proliferation and migration, but it suppressed cell apoptosis. Additionally, a reverse correlation between miR-31-5p and TNS1 regarding the expression level was identified, and TNS1 was verified to be a direct target of miR-31-5p. Besides, it was further validated by the rescue experiments that the tumor-promoting effects of miR-31-5p on LUAD cell functions were attenuated by TNS1 overexpression to some extent. The results based on the tumor xenograft experiment revealed that LUAD cell growth could be facilitated by miR-31-5p via the TNS1/p53 axis. Conclusion miR-31-5p facilitates LUAD cell progression mediated by the TNS1/p53 axis.
引用
收藏
页码:304 / 314
页数:11
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