α-Enolase Lies Downstream of mTOR/HIF1α and Promotes Thyroid Carcinoma Progression by Regulating CST1

Yang Liu; Lida Liao; Changming An; Xiaolei Wang; Zhengjiang Li; Zhengang Xu; Jie Liu; Shaoyan Liu

doi:10.3389/fcell.2021.670019

α-Enolase Lies Downstream of mTOR/HIF1α and Promotes Thyroid Carcinoma Progression by Regulating CST1

Front Cell Dev Biol. 2021 Apr 21:9:670019. doi: 10.3389/fcell.2021.670019. eCollection 2021.

Authors

Yang Liu¹, Lida Liao¹, Changming An¹, Xiaolei Wang¹, Zhengjiang Li¹, Zhengang Xu¹, Jie Liu¹, Shaoyan Liu¹

Affiliation

¹ Department of Head and Neck Surgical Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

Abstract

Novel therapy strategies are crucial for thyroid carcinoma treatment. It is increasingly important to clarify the mechanism of thyroid carcinoma progression. Several studies demonstrate that α-Enolase (ENO1) participates in cancer development; nevertheless, the role of ENO1 in thyroid carcinoma progression remains unclear. In the present study, we found that the expression of ENO1 was upregulated in thyroid carcinoma samples. Proliferation and migration of thyroid carcinoma cells were suppressed by depletion of ENO1; conversely, ENO1 overexpression promoted thyroid carcinoma cell growth and invasion. To elucidate the mechanisms, we found that the hypoxia-related mTOR/HIF1 pathway regulated ENO1 expression. ENO1 regulated the expression of CST1; knockdown of CST1 reversed the tumorigenicity enhanced by ENO1 overexpression. Taken together, our findings provide a theoretical foundation for thyroid carcinoma treatment.

Keywords: CST1; ENO1; HIF1α; mTOR; thyroid carcinoma.