α-烯醇化酶位于mTOR/HIF1α下游，并通过调节CST1促进甲状腺癌进展。

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

作者信息

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

机构信息

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.

出版信息

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

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.

新型治疗策略对甲状腺癌的治疗至关重要。阐明甲状腺癌进展机制变得越来越重要。多项研究表明，α-烯醇化酶（ENO1）参与癌症发展；然而，ENO1在甲状腺癌进展中的作用仍不清楚。在本研究中，我们发现ENO1在甲状腺癌样本中的表达上调。ENO1的缺失抑制了甲状腺癌细胞的增殖和迁移；相反，ENO1的过表达促进了甲状腺癌细胞的生长和侵袭。为了阐明其机制，我们发现缺氧相关的mTOR/HIF1途径调节ENO1的表达。ENO1调节CST1的表达；CST1的敲低逆转了ENO1过表达增强的致瘤性。综上所述，我们的研究结果为甲状腺癌的治疗提供了理论基础。