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

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 prog...

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Main Authors: Yang Liu, Lida Liao, Changming An, Xiaolei Wang, Zhengjiang Li, Zhengang Xu, Jie Liu, Shaoyan Liu
Format: Article
Language:English
Published: Frontiers Media S.A. 2021-04-01
Series:Frontiers in Cell and Developmental Biology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fcell.2021.670019/full
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spelling doaj-5b48b291b71d479f91941f8972c854d42021-04-21T05:37:48ZengFrontiers Media S.A.Frontiers in Cell and Developmental Biology2296-634X2021-04-01910.3389/fcell.2021.670019670019α-Enolase Lies Downstream of mTOR/HIF1α and Promotes Thyroid Carcinoma Progression by Regulating CST1Yang LiuLida LiaoChangming AnXiaolei WangZhengjiang LiZhengang XuJie LiuShaoyan LiuNovel 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.https://www.frontiersin.org/articles/10.3389/fcell.2021.670019/fullENO1thyroid carcinomaCST1mTORHIF1α
collection DOAJ
language English
format Article
sources DOAJ
author Yang Liu
Lida Liao
Changming An
Xiaolei Wang
Zhengjiang Li
Zhengang Xu
Jie Liu
Shaoyan Liu
spellingShingle Yang Liu
Lida Liao
Changming An
Xiaolei Wang
Zhengjiang Li
Zhengang Xu
Jie Liu
Shaoyan Liu
α-Enolase Lies Downstream of mTOR/HIF1α and Promotes Thyroid Carcinoma Progression by Regulating CST1
Frontiers in Cell and Developmental Biology
ENO1
thyroid carcinoma
CST1
mTOR
HIF1α
author_facet Yang Liu
Lida Liao
Changming An
Xiaolei Wang
Zhengjiang Li
Zhengang Xu
Jie Liu
Shaoyan Liu
author_sort Yang Liu
title α-Enolase Lies Downstream of mTOR/HIF1α and Promotes Thyroid Carcinoma Progression by Regulating CST1
title_short α-Enolase Lies Downstream of mTOR/HIF1α and Promotes Thyroid Carcinoma Progression by Regulating CST1
title_full α-Enolase Lies Downstream of mTOR/HIF1α and Promotes Thyroid Carcinoma Progression by Regulating CST1
title_fullStr α-Enolase Lies Downstream of mTOR/HIF1α and Promotes Thyroid Carcinoma Progression by Regulating CST1
title_full_unstemmed α-Enolase Lies Downstream of mTOR/HIF1α and Promotes Thyroid Carcinoma Progression by Regulating CST1
title_sort α-enolase lies downstream of mtor/hif1α and promotes thyroid carcinoma progression by regulating cst1
publisher Frontiers Media S.A.
series Frontiers in Cell and Developmental Biology
issn 2296-634X
publishDate 2021-04-01
description 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.
topic ENO1
thyroid carcinoma
CST1
mTOR
HIF1α
url https://www.frontiersin.org/articles/10.3389/fcell.2021.670019/full
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