Knockdown of UACA inhibitsproliferation and invasion and promotes senescence of hepatocellular carcinoma cells

Uveal autoantigen with coiled-coil domains and ankyrin repeats (UACA/Nucling), has been reported to be upregulated in various cancers. However, its expression and function have not been studied in hepatocellular carcinoma (HCC). In the present study, expression of UACA was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and the results revealed that UACA was upregulated in 23 cases of HCC compared with paired corresponding non-tumor liver tissues. In addition, the upregulation of UACA in HCC was further validated by analyzing the datasets from The Cancer Genome Atlas-Liver Hepatocellular Carcinoma (TCGA-LIHC) and GSE36376. Furthermore, knockdown of UACA suppressed the proliferative and invasive ability as well as inducing senescence of HCC cells. Besides, the expression level of UACA was positively associated with Hif1α (hypoxia-inducible factor 1α) in HCC datasets from TCGA-LIHC and GSE54236. Moreover, treatment with CoCl led to the increased expression and the localization alteration of UACA in HCC cells. In summary, UACA is upregulated in HCC and knockdown of UACA ameliorated malignant behaviors of HCC cells, and UACA was correlated with and under control of Hif1α.