Published online Nov 21, 2019. doi: 10.3748/wjg.v25.i43.6386
Peer-review started: January 16, 2019
First decision: February 13, 2019
Revised: September 10, 2019
Accepted: September 13, 2019
Article in press: September 13, 2019
Published online: November 21, 2019
Processing time: 309 Days and 18.3 Hours
Hepatocellular carcinoma (HCC) is one of most common malignant tumors with a poor prognosis. Increasing studies indicated that dysregulation of ubiquitin-conjugating enzyme E2T (UBE2T) contributes to the development of human cancers. However, whether UBE2T is involved in the progression of HCC is unclear.
Previous studies have illustrated the critical role of UBE2T in the progression of various tumors, and our study will suggest the role of UBE2T in regulating the occurrence and development of HCC.
To investigate the biological function of UBE2T in HCC cell proliferation and progression in vitro by gain-of-function and loss-of-function strategies, and provides significant insights into the underlying molecular mechanisms of UBE2T involved in the development of HCC, which may contribute to the future research of more effective diagnosis and treatment.
The expression of UBE2T in HCC tissues was obtained from The Cancer Genome Atlas database. In vitro experiments using lentivirus-medicated approach were performed to examine cell growth, cell cycle distribution, and apoptosis by CCK8 assay and flow cytometry, respectively. The xenograft tumorigenicity assay was performed to determine the capacity of cell proliferation in vivo. The whole genome expression profile was analyzed by microarray assay.
In this study, we identified remarkable overexpression of UBE2T in HCC tissues, which closely corrected with a poor overall survival in HCC patients. The results of in vitro experiments suggested a critical role of UBE2T in cell viability, cell cycle, and apoptosis of HCC. In both SMMC-7721 and BEL-7404 cells, the HCC cell proliferation was obviously inhibited, cell cycle was arrested at G1/S phase, and apoptosis was significantly promoted by lentivirus-medicated UBE2T knockdown. Moreover, the growth of SMMC-7721 cells with UBE2T knockdown in xenografts was significantly inhibited in vivo. The microarray assay confirmed that UBE2T silencing contributed to the dysregulation of numerous genes, including IL-1B, FOSL1, PTGS2, and BMP6.
In conclusion, UBE2T is significantly involved in HCC cell proliferation, cell cycle, and apoptosis.
Our study may provide a novel potential diagnostic and therapeutic target for HCC intervention.