Wang Lisi, Xiao Xiaolong, Du Hong
Department of Respiratory and Critical Care Medicine, Chongqing People's Hospital, Chongqing, 400013, People's Republic of China.
Shanghai Engineering Research Center of Pharmaceutical Translation, Shanghai, 200231, People's Republic of China.
Mol Biotechnol. 2022 May;64(5):526-534. doi: 10.1007/s12033-021-00446-0. Epub 2022 Jan 8.
To study the modulatory mechanism of let-7c-5p on the biological characteristics of lung adenocarcinoma (LUAD) cells by targeting AURKB. Differentially expressed genes (DEGs) were screened by bioinformatics analysis. CCK-8, colony formation, scratch healing, Transwell, and flow cytometry assays were employed to test biological functions of LUAD cells. Western Blot was undertaken to assay the protein level of AURKB, and qRT-PCR was undertaken to test AURKB mRNA and let-7c-5p expression. Dual-luciferase reporter gene method was applied to detect the interaction between AURKB and let-7c-5p. Let-7c-5p was much likely to target AURKB expression. Let-7c-5p was poorly expressed in LUAD cells and suppressed AURKB. Silencing AURKB or overexpressing let-7c-5p both could suppress proliferation, migration, and invasion and stimulate apoptosis, while overexpressing the two simultaneously could reverse such effect. Forced expression of let-7c-5p inhibited proliferation, migration, and invasion and accelerated apoptosis of LUAD cells by inhibiting AURKB, which may provide a new way to understand the malignant progression of LUAD.
通过靶向AURKB研究let-7c-5p对肺腺癌（LUAD）细胞生物学特性的调控机制。通过生物信息学分析筛选差异表达基因（DEG）。采用CCK-8、集落形成、划痕愈合、Transwell和流式细胞术检测LUAD细胞的生物学功能。进行蛋白质免疫印迹法检测AURKB的蛋白水平，进行qRT-PCR检测AURKB mRNA和let-7c-5p的表达。应用双荧光素酶报告基因法检测AURKB与let-7c-5p之间的相互作用。Let-7c-5p很可能靶向AURKB的表达。Let-7c-5p在LUAD细胞中低表达并抑制AURKB。沉默AURKB或过表达let-7c-5p均可抑制增殖、迁移和侵袭并促进凋亡，而同时过表达二者可逆转这种效应。强制表达let-7c-5p通过抑制AURKB抑制LUAD细胞的增殖、迁移和侵袭并加速其凋亡，这可能为理解LUAD的恶性进展提供新途径。
