Abstract
The present study aimed to explore the role of ubiquitin-conjugating enzyme E2 C (UBE2C) in the progress of thyroid carcinoma (THCA). We firstly explored the prognostic impact and expression level of UBE2C in THCA. Then, we performed the UBE2C knockdown and evaluated the effects on the proliferation, cell cycle distribution, apoptosis, migration, and invasion of THCA cells, as well as resistance to sorafenib. Finally, we predicted the possible pathways and explored the correlation between UBE2C with immune infiltrates. The results showed that high expression of UBE2C independently predicted a shorter disease-free survival time of THCA patients. And UBE2C also presented a better prognostic performance on the survival probability of patients. Expression analysis showed that UBE2C was statistically upregulated in THCA tissue compared with normal tissue. After UBE2C knockdown, the proliferation of THCA cells was inhibited and apoptosis was increased. These results indicated that UBE2C acted as an oncogene in THCA. However, the migration and invasion of THCA cells with UBE2C knockdown were enhanced, and the expressions of migration-related proteins were upregulated. In addition, UBE2C knockdown increased the resistance of THCA cells to sorafenib. These results implied the potential of UBE2C as a suppressor gene in THCA. The pathway analysis further predicted that metabolism-related pathways were activated in the UBE2C low expression class, and cell growth and immune-related pathways were focused on the UBE2C high expression class. Finally, we observed a significant positive relationship between UBE2C and several immune infiltrates in THCA. It followed that UBE2C high expression might play a vital role in THCA to some extent. This study revealed that UBE2C participated in the progression of THCA and may play the dual role of both oncogene and tumor suppressor gene. The detailed mechanism needed to be further investigated.
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