Objectives FAM83A is recently found to be overexpressed in cancer and hypothesized to be oncogenic. This study is to illustrate the functional role and mechanism of FAM83A in cervical cancer.
Methods 153 different clinical cervical specimens were used for validation by SYBR Green RT-qPCR and IHC. Cell proliferation, cell migration and invasion were done for functional validation. RNA-seq approach was applied to investigate the altered genes regulated by FAM83A.
Results We found FAM83A is overexpressed in cervical cancer tissues. However, the expression of FAM83A was instead decreased in patients with advanced FIGO stage, deep stromal invasion, poor differentiation and/or lymph node metastasis, and negatively associated with short survival of patients with cervical cancer. We found knockdown of FAM83A increased cervical cancer cell proliferation, promoted cell migration and invasion. We further identified 192 genes that were changed in the context of FAM83A knockdown. KEGG pathway analysis showed ECM-receptor interaction, focal adhesion, PI3K-Akt signaling and TNF signaling were the main activated pathways.
Conclusions We conclude that FAM83A exerts an unexpected tumor suppressive role in cervical cancer progression.
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