P Han1, X-H Wang, Y-F Han, G-M Chen. 1. Department of Respiratory (II), Linyi People's Hospital, Linyi, P.R. China. xiaochen893@163.com.
Abstract
OBJECTIVE: To investigate the effect of miR-140 on migration and invasion of non-small cell lung cancer (NSCLC) A549 cell and its regulatory mechanism. MATERIALS AND METHODS: The NSCLC cell lines A549, H1650, NCI-H838, and normal lung epithelial cells BEAS-2B were purchased, and the expression of miR-140 and Smad3 in cells was detected by RT-PCR. MiR-140-inhibitor, miR-140-mimincs, miR-NC, sh-Smad3, Si-Smad3, and NC were transfected into A549 cells. Quantitative Real Time-Polymerase Chain Reaction (QRT-PCR) was used to detect the expression of miR-140 and Smad3. Transwell and cell scratch assay were used to detect cell invasion and migration. Dual-Luciferase report assay was used to study the relationship between mir-140 and Smad3. RESULTS: MiR-140 was lowly expressed and Smad3 was highly expressed in NSCLC cells. Cell researches showed that the overexpression of miR-140 can inhibit cell invasion and migration. The downregulation of Smad3 expression inhibits cell invasion and migration. Dual-Luciferase reporter assay showed that miR-140 is a Smad3 targeting site. CONCLUSIONS: MiR-140 can inhibit the invasion and migration of NSCLC cells by regulating Smad3, and it is expected to become a potential clinical target.
OBJECTIVE: To investigate the effect of miR-140 on migration and invasion of non-small cell lung cancer (NSCLC) A549 cell and its regulatory mechanism. MATERIALS AND METHODS: The NSCLC cell lines A549, H1650, NCI-H838, and normal lung epithelial cells BEAS-2B were purchased, and the expression of miR-140 and Smad3 in cells was detected by RT-PCR. MiR-140-inhibitor, miR-140-mimincs, miR-NC, sh-Smad3, Si-Smad3, and NC were transfected into A549 cells. Quantitative Real Time-Polymerase Chain Reaction (QRT-PCR) was used to detect the expression of miR-140 and Smad3. Transwell and cell scratch assay were used to detect cell invasion and migration. Dual-Luciferase report assay was used to study the relationship between mir-140 and Smad3. RESULTS:MiR-140 was lowly expressed and Smad3 was highly expressed in NSCLC cells. Cell researches showed that the overexpression of miR-140 can inhibit cell invasion and migration. The downregulation of Smad3 expression inhibits cell invasion and migration. Dual-Luciferase reporter assay showed that miR-140 is a Smad3 targeting site. CONCLUSIONS:MiR-140 can inhibit the invasion and migration of NSCLC cells by regulating Smad3, and it is expected to become a potential clinical target.