The function of miR-637 in non-small cell lung cancer progression and prognosis

被引:11
作者
Jia, Teng [1 ]
Zhang, Qingguang [1 ]
Xu, Haitao [1 ]
Liu, Hongjian [1 ]
Gu, Xiaojie [2 ]
机构
[1] Binzhou Med Univ Hosp, Dept Thorac Surg, Binzhou 256003, Shandong, Peoples R China
[2] Binzhou Med Univ Hosp, Dept Ultrasound, 661 Huanghe 2nd Rd, Binzhou 256003, Shandong, Peoples R China
关键词
Non-small cell lung cancer; Prognosis; miR-637; Biomarker; UNFAVORABLE PROGNOSIS; MICRORNA; INVASION; PROLIFERATION; TUMORIGENESIS; RECURRENCE; EXPRESSION; MIRNA-637; MIGRATION; NSCLC;
D O I
10.1016/j.pulmoe.2021.05.005
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
Background: Non-small cell lung cancer (NSCLC) is the most common type of lung cancer with a high mortality rate and poor prognosis. miR-637 has been reported to regulate tumor progression and act as a prognosis biomarker of various cancers. Its functional role in NSCLC was investigated in this study. Methods: The expression level of miR-637 in NSCLC tissues and adjacent normal tissues of 123 NSCLC patients was analyzed by qRT-PCR. The association between miR-637 and clinical patho-logical features in the prognosis of patients was analyzed. Cell transfection was performed to overexpress or knockdown miR-637 in H1299 and HCC827. The proliferation, migration, and inva-sion of H1299 and HCC827 were evaluated by CCK8 and Transwell assay. Results: miR-637 expression was significantly decreased in NSCLC tissues and cell lines relative to normal tissues and cells. The survival rate of NSCLC patients with low miR-637 expression was lower than that of patients with high miR-637 expression. Additionally, miR-637 served as a tumor suppressor that inhibited cell proliferation, migration, and invasion of NSCLC. Conclusion: Downregulation of miR-637 in NSCLC was associated with TNM stage and poor prog-nosis of patients and served as a tumor suppressor in NSCLC. These results provide a potential strategy to control NSCLC. & COPY; 2021 Sociedade Portuguesa de Pneumologia. Published by Elsevier Espana, S.L.U. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
引用
收藏
页码:111 / 118
页数:8
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