Fu Jiajia, Li Tong, Jiang Xiaozhen, Xia Bin, Hu Lijuan
Department of Pulmonary Medicine, The Second People's Hospital of Yueqing, Zhejiang, 325608 China.
Department of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai, 200032 China.
3 Biotech. 2021 Jul;11(7):352. doi: 10.1007/s13205-021-02881-x. Epub 2021 Jun 22.
The present study was undertaken to study the function of miRNA-199-3p in the regulation of human lung cancer growth and metastasis. The results showed significant ( < 0.05) downregulation of miRNA-199-3p in lung cancer tissues and cell lines. Overexpression of miR-197 caused considerable inhibition of the viability and colony formation of the lung cancer cells. The inhibition of proliferation was found to be due to the arrest of the SK-LU-1 lung cancer cells. At the G/M phase of the cell cycle. In silico analysis and subsequent the dual-luciferase assays showed that miR-199-3p targets Sp1 at molecular. The expression of Sp1 was significantly ( < 0.05) upregulated in lung cancer cells and tissues. Nonetheless, miR-199-3p overexpression could cause post-transcriptional suppression of Sp1. Silencing of Sp1suppress the proliferation of SK-LU-1 lung cancer cells. However, overexpression Sp1 transcription factor prevents the tumor-suppressive effects of miR-199-3p on lung cancer cells. Additionally, miR-199-3p was found to suppresses the migration, invasion and epithelial-to-mesenchymal transition of human lung cancer cells. Summing up, miRNA-199-3p/SP1 axis controls the growth and metastasis of SK-LU-1 lung cancer cells.
本研究旨在探讨miRNA-199-3p在调控人肺癌生长和转移中的作用。结果显示,肺癌组织和细胞系中miRNA-199-3p显著下调(<0.05)。miR-199-3p过表达导致肺癌细胞活力和集落形成受到显著抑制。发现增殖抑制是由于SK-LU-1肺癌细胞在细胞周期的G/M期停滞所致。计算机分析及随后的双荧光素酶检测表明,miR-199-3p在分子水平上靶向Sp1。Sp1在肺癌细胞和组织中的表达显著上调(<0.05)。尽管如此,miR-199-3p过表达可导致Sp1的转录后抑制。Sp1沉默可抑制SK-LU-1肺癌细胞的增殖。然而,Sp1转录因子过表达可阻止miR-199-3p对肺癌细胞的肿瘤抑制作用。此外,发现miR-199-3p可抑制人肺癌细胞的迁移、侵袭和上皮-间质转化。综上所述,miRNA-199-3p/SP1轴控制SK-LU-1肺癌细胞的生长和转移。