GSE108500
Knockdown of FOXP1 promotes the development of lung adenocarcinoma
Lung cancer is one of the most common cancers in the world, which accounts for about 27% of all cancer deaths. However, the mechanisms underlying the pathogenesis of lung cancer cells remain largely elusive. In this study, we examined the role of the Forkhead box protein P1 (FOXP1) in lung cancer development. Our Oncomine analysis shows that FOXP1 is downregulated in lung adenocarcinoma compared with normal lung tissue. Knockdown of FOXP1 promotes the proliferation growth and invasion of PC9 and A549 cells by regulating genes of chemokine signaling molecules, including CCR1, ADCY5, GNG7, VAV3, and PLCB1. Simultaneous knockdown of CCR1 and FOXP1 attenuated FOXP1 knockdown-induced increase of lung cancer cell growth. Finally, knockdown of FOXP1 in PC9 cells promotes the tumorigenesis via CCR1 signaling in xenograft mouse model. Taken together, our data suggest that FOXP1 plays important roles in preventing lung adenocarcinoma development via suppressing chemokine signaling pathways. Novel strategies might be developed to prevent the development of lung adenocarcinoma by targeting FOXP1 Overall design: Three control and three FOXP1 knockdown A549 cell lines were subjected to RNA sequencing. Total RNA was extracted 48 h after the FOXP1siRNA or control siRNA transfected. With the RNA sequencing data prepared, the expression abundance (FPKM) value of each gene was estimated by running cufflinks and the differential expressed genes were assessed by cuffdiff. Only those genes with |fold change|> 2 and adjusted p value < 0.01 were recognized as statistically differentially expressed between two groups. The adjusted p value was obtained through applying Benjamini and Hochberg's (BH) false discovery rate correction on the original p value, and fold change threshold was selected based on our purpose of focusing on significantly differentially expressed genes.