Bromodomain‑containing protein 4 is critical for the antiproliferative and pro‑apoptotic effects of gambogic acid in anaplastic thyroid cancer
- Yonghui Wang
- Wei Wang
- Hongqin Sun
Affiliations: Department of Breast Surgery, Weifang People's Hospital, Weifang, Shandong 261041, P.R. China, Department of Breast, Thyroid and Hernia Surgery, Liaocheng People's Hospital, Liaocheng, Shandong 252000, P.R. China, Department of Central Sterile Supply, Weifang People's Hospital, Weifang, Shandong 261041, P.R. China
- Published online on: April 26, 2018 https://doi.org/10.3892/ijmm.2018.3642
Copyright: © Wang
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Gambogic acid (GA) has been widely used as an anticancer drug for different tumors, including thyroid cancer. However, the potential function and molecular mechanisms of GA in anaplastic thyroid cancer (ATC) has not been illustrated thus far. The aim of the present study was to demonstrate the antitumor effects of GA on ATC cells and investigate its underlying molecular mechanisms. The results revealed that GA significantly decreased the viability and proliferation, as well as induced cell apoptosis in ATC cell lines. Next, it was demonstrated that GA decreased the expression of bromodomain‑containing protein 4 (BRD4), which has been reported to function as an oncogene in various types of cancer. BRD4 expression was significantly higher in ATC tissues compared with that in adjacent normal thyroid tissues. In addition, BRD4 silencing significantly repressed the cell viability and proliferation, and increased the cell apoptotic rate in vitro, while it also delayed the tumor growth in vivo. Notably, ectopic BRD4 expression significantly weakened the biological effects of GA on ATC cells in vitro and in vivo, which suggested that GA served its anticancer functions partially via downregulating BRD4. In conclusion, BRD4, functioning as an oncogene in ATC, is important for the antiproliferative and pro‑apoptotic effects of GA.