Upregulation of FAM83D promotes malignant phenotypes of lung adenocarcinoma by regulating cell cycle.

The family with sequence similarity 83, member D (FAM83D) gene is upregulated in hepatocellular carcinoma and ovarian cancer, and its overexpression has been reported to positively correlate with tumor progression. However, the clinical significance and biological function of FAM83D in lung adenocarcinoma has not been investigated. We determined the expression profile and clinical significance of FAM83D using The Cancer Genome Atlas (TCGA) and immunohistochemistry (IHC) analysis. Considerable upregulation of FAM83D was observed in LUAD tissues compared with adjacent normal tissues, and its overexpression was significantly associated with more advanced clinicopathological characteristics. Importantly, multivariate Cox regression analysis indicated that a high level of FAM83D expression was an independent risk factor for worse overall survival in LUAD patients (HR = 1.692, P = 0.006). Inhibition of FAM83D suppressed the proliferation of LUAD cells via G1 phase arrest by downregulating cyclin D1 (CCND1) and cyclin E1 (CCNE1). The oncogenic role of FAM83D was also confirmed in vivo. In conclusion, our study demonstrated that FAM83D might exert its oncogenic activity in LUAD by regulating cell cycle, and that it could serve as a novel biomarker and a potential therapeutic target for LUAD.