Abstract：Objective To detect the regulatory effect of miR-320a on the epithelial-mesenchymal transition of non-small cell lung cancer cells and the possible mechanism.Methods Sixty patients with NSCLC who were hospitalized and received surgery in our hospital between July 2017 and December 2018 were selected as subjects. The resected cancer tissues and adjacent tissues were taken intraoperatively.The expressions of miR-320a and FoxM1in cancer tissues and adjacent tissues were detected by RT-PCR and Western blot. A549 cells were transfected with miR-320a mimics, miR-320a NC, and miR-320a inhibitor. Twenty-four hours after transfection, scratches and Transwellwere performed to test the migration and invasion ability of cells in each group. The dual luciferase reporter gene system was used to predict the targeting relationship between miR-320a and FoxM1. Western blot was used to detect the expressions of FoxM1, E-Cadherin and Vimentin proteins in each group of cells.Results The relative expression of miR-320a in adjacent tissues was significantly higher than that in cancerous tissues (P<0.001), and the positive cell rate of FoxM1 was significantly higher than in adjacent tissues (P<0.001). The expression of miR-320a in patients with TNM stage Ⅰ to Ⅱ was significantly higher than that in patients with Ⅲ to Ⅳ. The expression of miR-320a in poorly differentiated cancer tissues was significantly lower than that in moderately and highly differentiated cancer tissues. The migration and invasion abilityof cells in MiR-320a NC group was poorer than that of miR-320a mimics group (P<0.001), but better than that of miR-320a inhibitor group (P<0.001). The dual luciferase reporter gene proved that miR-320a could down-regulate FoxM1 expression. The expression of E-cadherin in miR-320a mimics FoxM1-WT A549 group was significantly higher than that in miR-320a NC group (P<0.001), but the expression of Vimentin was significantly lower (P<0.001). The expression of E-cadherin in inhibitor group was significantly lower than that in miR-320a NC group (P<0.001), but the expression of Vimentin was significantly higher (P<0.001).Conclusions miR-320a may play the role of a tumor suppressor gene in non-small cell lung cancer. This effect may be achieved via targeted inhibition of FoxM1 expression, thereby inhibiting the epithelial-mesenchymal transition process of non-small cell lung cancer cells.
Li Qin-Qin, Zhang Le, Wan Hai-Ying, et al. CREB1-driven expression of miR-320a promotes mitophagy by down-regulating VDAC1 expression during serum starvation in cervical cancer cells[J]. Oncotarget, 2015, 6(33): 34924-34940.
Zhu Y, Zhang Y, Sui Z H, et al. USP14 de-ubiquitinates vimentin and miR-320a modulates USP14 and vimentin to contribute to malignancy in gastric cancer cells[J]. Oncotarget, 2014, 8(30):48725-48736.
Shi C, Zhang Z. MicroRNA-320 suppresses cervical cancer cell viability, migration and invasion via directly targeting FOXM1[J]. Oncol Left, 2017, 14(3):3809-3816.
[21]
Wan L Y, Deng J, Xiang X J, et al. miR-320 enhances the sensitivity of human colon cancer cells to chemoradiotherapy in vitro by targeting FOXM1[J]. Biochem Bioph Res Co, 2015, 457(2):125-132.
2020, Vol. 31 
