No.1 Department of Respiratory and Critical Care Medicine, Cangzhou Central Hospital, No. 16, Xinhua West Road, Yunhe District, Cangzhou City, Hebei Province, China.
Department of No. 1 Pediatrics, Cangzhou Hospital of Integrated TCM-WM, Cangzhou City, Hebei Province, China.
Bioengineered. 2021 Dec;12(2):11959-11977. doi: 10.1080/21655979.2021.2009422.
MicroRNA (miR)-140-3p has been proved to repress lung adenocarcinoma (LUAD), and our study aims to further evaluate the mechanism. Bioinformatic analyses were performed. The viability, proliferation, migration, invasion and angiogenesis of transfected LUAD cells were all determined via Cell Counting Kit-8, colony formation, Scratch, Transwell, and tube formation assays. The targeting relationship between miR-140-3p and thymidylate synthetase (TYMS) was confirmed by dual-luciferase reporter assay. Relative expressions of miR-140-3p, TYMS, epithelial-to-mesenchymal transition- (E-cadherin, N-cadherin, vimentin), angiogenesis- (vascular endothelial growth factor (VEGF)), and apoptosis-related factors (cleaved caspase-3, B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax)) were quantified by quantitative real-time polymerase chain reaction or Western blot. TYMS was high-expressed yet miR-140-3p was low-expressed in LUAD cells. Upregulation of miR-140-3p inhibited TYMS expression, viability, colony formation, migration, invasion, and tube length within LUAD cells, while downregulation of miR-140-3p did oppositely. Silenced TYMS, the downstream target gene of miR-140-3p, reversed the effects of miR-140-3p downregulation on TYMS expression, cell viability, colony formation, migration, invasion, and tube length as well as the metastasis-, apoptosis- and angiogenesis-related proteins in LUAD cells. Upregulation of miR-140-3p inhibited the proliferation, migration, invasion and angiogenesis of LUAD cells via targeting TYMS.
微小 RNA(miR)-140-3p 已被证明可抑制肺腺癌(LUAD),我们的研究旨在进一步评估其机制。进行了生物信息学分析。通过细胞计数试剂盒-8、集落形成、划痕、Transwell 和管形成测定来确定转染的 LUAD 细胞的活力、增殖、迁移、侵袭和血管生成。通过双荧光素酶报告基因测定证实了 miR-140-3p 和胸苷酸合成酶(TYMS)之间的靶向关系。通过定量实时聚合酶链反应或 Western blot 定量 miR-140-3p、TYMS、上皮-间充质转化(E-cadherin、N-cadherin、vimentin)、血管生成(血管内皮生长因子(VEGF))和凋亡相关因子(cleaved caspase-3、B 细胞淋巴瘤-2(Bcl-2)、Bcl-2 相关 X 蛋白(Bax))的相对表达。在 LUAD 细胞中,TYMS 高表达而 miR-140-3p 低表达。上调 miR-140-3p 抑制 TYMS 表达、LUAD 细胞活力、集落形成、迁移、侵袭和管长度,而下调 miR-140-3p 则相反。沉默 TYMS,miR-140-3p 的下游靶基因,逆转了 miR-140-3p 下调对 TYMS 表达、细胞活力、集落形成、迁移、侵袭和管长度以及 LUAD 细胞中转移、凋亡和血管生成相关蛋白的影响。上调 miR-140-3p 通过靶向 TYMS 抑制 LUAD 细胞的增殖、迁移、侵袭和血管生成。
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