UHRF1 Induces Metastasis in Thyroid Cancer

Bo-Hua Kuang; Guo-He Lin; Quentin Liu; Bi-Cheng Wang

doi:10.1155/2022/7716427

UHRF1 Induces Metastasis in Thyroid Cancer

J Oncol. 2022 Aug 13:2022:7716427. doi: 10.1155/2022/7716427. eCollection 2022.

Authors

Bo-Hua Kuang¹, Guo-He Lin², Quentin Liu^{3

4}, Bi-Cheng Wang¹

Affiliations

¹ Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
² Department of Oncology, The Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, China.
³ State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-Sen University, Guangzhou 510060, China.
⁴ Institute of Cancer Stem Cell, Dalian Medical University, Dalian 116044, China.

Abstract

Background: Ubiquitin-like with PHD and ring-finger domain 1 (UHRF1) has been defined as an oncogene in tumor cells. However, the role of UHRF1 in mediating metastasis in thyroid cancer remains unexplored. In this study, we aimed to investigate the metastatic function and the potential mechanisms of UHRF1 in thyroid cancer.

Methods: Transwell assays were used to detect the metastatic capability of thyroid cancer. Dual-luciferase reporter assays were applied to examine the activation of transcription factors. Coimmunoprecipitation assays and immunofluorescence staining assays were used to elucidate the potential mechanisms of UHRF1 in promoting the metastasis of thyroid cancer.

Results: In this study, we found that overexpression of UHRF1 promoted the metastasis of papillary thyroid cancer cells, and suppression of UHRF1 decreased the metastasis of anaplastic thyroid cancer cells. Regarding the signaling pathway in regulating metastasis, UHRF1 directly combined and activated the transcription factor c-Jun/AP-1 in the nucleus, subsequently increasing the transcription of IL-6 and MIF.

Conclusion: Our results suggest that UHRF1 could induce the metastasis of thyroid cancer, and the potential signaling pathway might be that UHRF1 activates c-Jun/AP-1 to increase the expression of IL-6 and MIF. These findings provide a novel mechanism of UHRF1 and illustrate that UHRF1/AP-1 complex could be a potential therapeutic target for patients with thyroid cancer.