FAM83A exerts tumor‑suppressive roles in cervical cancer by regulating integrins.

Abstract

Family with sequence similarity 83 member A (FAM83A) has been recently observed to be upregulated in various types of cancer and hypothesized to be serve as an oncogene. The present study aimed to determine the functional roles and the underlying molecular mechanism of FAM83A in cervical cancer. The results demonstrated that although FAM83A expression was increased in cervical cancer compared with normal tissues, the expression levels of FAM83A were decreased in patients with advanced FIGO stage, deep stromal invasion, poor differentiation and/or lymph node metastasis and negatively associated with short survival time of patients with cervical cancer. FAM83A knockdown promoted cell proliferative, migratory and invasive abilities of CaSki and HeLa cells. A mouse xenograft model demonstrated that FAM83A knockdown promoted tumor growth in vivo. Mechanistically, RNA sequencing results revealed that knockdown of FAM83A increased the transcription of genes mainly associated with oncogenesis-associated pathways. In addition, FAM83A knockdown increased the protein levels of α1, α3, α5, β4 and β5 integrins in vitro and in vivo, and the expression of FAM83A was also negatively associated with the levels of these proteins in human cervical cancer tissue samples. In conclusion, the results of the present study suggested that FAM83A may exert a tumor-suppressive role in cervical cancer by suppressing the expression of integrins, which may offer new insight into the biological basis of cervical cancer.