High level of FANCI correlates with worse prognostic outcome and promotes tumor growth of lung adenocarcinoma partly by suppressing the activation of M1 macrophages

Abstract FANCI, as a member of the Fanconi anemia (FA) complementation group, normally associates with FANCD2 to play an important role in ribosome biogenesis and DNA repair. However, the correlation of FANCI to prognostic value and the molecular mechanism in lung adenocarcinoma (LUAD) patients remain unclear. In the present paper, bioinformatics analysis was performed on LUAD data from TCGA and GEO database, and further to be confirmed by in vitro experiment. We found that high level of FANCI was significantly correlated with worse survival probability of LUAD patients. Moreover, the results from in vitro experiments revealed that high levels of FANCI were found in LUAD specimens and LUAD cell lines. Knockdown the expression of FANCI in A549 cells and H460 cells significantly inhibited the cell viability and clone formation of LUAD cells in vitro and in vivo. Furthermore, high FANCI level was negatively correlated with a variety of the tumor infiltrating immune cells. Importantly, overexpression of FANCI significantly inhibited the activation of M1 macrophages. All the data demonstrated that FANCI was a useful prognostic biomarker in LUAD patients and knockdown FANCI inhibited tumor growth of LUAD cells in vitro and in vivo partly by suppressing the activation of M1 macrophages.