Effect of FGL1 on invasion and migration of lung adenocarcinoma cells induced by docetaxel and its mechanism / 中国药理学通报

ABSTRACT

Aim To investigate the effect of fibrinogen-isomeric protein 1 (FGL1) on the invasion and migration ability of docetaxel induced lung adenocarcinoma cells and the related mechanism. Methods Gene expression of FGL1 in tumors was obtained from TCGA database, and the Kaplan Meier Plotter database was used to analyze the sample information in the GEO database and draw the survival curve. The PC-9 and A549 of human lung adenocarcinoma cells were selected as the research object. FGL1 expression was knocked down by small interfering RNA (siRNA). Transwell method and cell scratch test were employed to detect cell invasion and migration; Western blot was applied to detect the expression level of E-cadherin and N-cadherin proteins. Results Compared with normal tissues, FGL1 expression was significantly up-regulated in lung adenocarcinoma. Survival analysis showed that the overall survival of patients with high FGL1 expression was shorter than that of patients with low expression. The migration and invasion ability of PC-9 and A549 cells significantly decreased after knockdown FGL1 expression. Under the same doze of docetaxel, decreased expression of FGL1 significantly inhibited the invasion and migration ability of lung adenocarcinoma PC-9 and A549 cells. FGL1 silencing combined with docetaxel significantly down-regulated N-cadherin protein expression and up-regulated E-cadherin protein expression in lung adenocarcinoma cells. Conclusions FGL1 is highly expressed in lung adenocarcinoma and is related to patient survival and prognosis. FGL1 can enhance the ability of docetaxel to inhibit the invasion and migration of lung adenocarcinoma PC-9 and A549 cells by blocking the EMT process.