Thyroid hormones inhibit tumor progression and enhance the antitumor activity of lenvatinib in hepatocellular carcinoma via reprogramming glucose metabolism

Abstract Thyroid hormones (THs) dysfunctions have been demonstrated to be associated with the risk of developing different types of cancers. The role of THs in regulating hepatocellular carcinoma (HCC) progression is still controversial. We demonstrated that T3 can inhibit HCC progression by enhanci...

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Main Authors: Chun‑Cheng Yang, Yu-Chuan Yan, Guo‑Qiang Pan, Guang-Xiao Meng, Xiao Zhang, Lun-Jie Yan, Zi-Niu Ding, Dong-Xu Wang, Rui-Zhe Li, Guang-Zhen Li, Zhao‑Ru Dong, Tao Li
Format: Article
Language:English
Published: Nature Publishing Group 2025-03-01
Series:Cell Death Discovery
Online Access:https://doi.org/10.1038/s41420-025-02378-z
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author Chun‑Cheng Yang
Yu-Chuan Yan
Guo‑Qiang Pan
Guang-Xiao Meng
Xiao Zhang
Lun-Jie Yan
Zi-Niu Ding
Dong-Xu Wang
Rui-Zhe Li
Guang-Zhen Li
Zhao‑Ru Dong
Tao Li
author_facet Chun‑Cheng Yang
Yu-Chuan Yan
Guo‑Qiang Pan
Guang-Xiao Meng
Xiao Zhang
Lun-Jie Yan
Zi-Niu Ding
Dong-Xu Wang
Rui-Zhe Li
Guang-Zhen Li
Zhao‑Ru Dong
Tao Li
author_sort Chun‑Cheng Yang
collection DOAJ
description Abstract Thyroid hormones (THs) dysfunctions have been demonstrated to be associated with the risk of developing different types of cancers. The role of THs in regulating hepatocellular carcinoma (HCC) progression is still controversial. We demonstrated that T3 can inhibit HCC progression by enhancing the expression of THRSP. Mechanistically, T3 can activate tumor suppressor LKB1/AMPK/Raptor signaling as well as oncogenic PI3K/Akt signaling in HCC. Interestingly, T3-induced THRSP can augment the activation of LKB1/AMPK/Raptor signaling, yet inhibit T3-induced PI3K/Akt signaling activation, thereby preventing mTOR-induced nuclear translocation of HIF-1α, and ultimately suppressing ENO2-induced glycolysis and HCC progression. More importantly, the exogenous T3 enhances the antitumor effect of multikinase inhibitor lenvatinib in vitro and in vivo by regulating glycolysis. Our findings reveal the role and mechanism of THs in HCC progression and glucose metabolism and provide new potential therapeutic strategies for HCC treatment and drug resistance reversal.
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publishDate 2025-03-01
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series Cell Death Discovery
spelling doaj-art-33db49e3ad9e4088a6a473b4d22cedd12025-08-20T02:59:23ZengNature Publishing GroupCell Death Discovery2058-77162025-03-0111111310.1038/s41420-025-02378-zThyroid hormones inhibit tumor progression and enhance the antitumor activity of lenvatinib in hepatocellular carcinoma via reprogramming glucose metabolismChun‑Cheng Yang0Yu-Chuan Yan1Guo‑Qiang Pan2Guang-Xiao Meng3Xiao Zhang4Lun-Jie Yan5Zi-Niu Ding6Dong-Xu Wang7Rui-Zhe Li8Guang-Zhen Li9Zhao‑Ru Dong10Tao Li11Department of General Surgery, Qilu Hospital, Shandong UniversityDepartment of General Surgery, Qilu Hospital, Shandong UniversityDepartment of General Surgery, Qilu Hospital, Shandong UniversityDepartment of General Surgery, Qilu Hospital, Shandong UniversityDepartment of General Surgery, Qilu Hospital, Shandong UniversityDepartment of General Surgery, Qilu Hospital, Shandong UniversityDepartment of General Surgery, Qilu Hospital, Shandong UniversityDepartment of General Surgery, Qilu Hospital, Shandong UniversityDepartment of General Surgery, Qilu Hospital, Shandong UniversityDepartment of General Surgery, Qilu Hospital, Shandong UniversityDepartment of General Surgery, Qilu Hospital, Shandong UniversityDepartment of General Surgery, Qilu Hospital, Shandong UniversityAbstract Thyroid hormones (THs) dysfunctions have been demonstrated to be associated with the risk of developing different types of cancers. The role of THs in regulating hepatocellular carcinoma (HCC) progression is still controversial. We demonstrated that T3 can inhibit HCC progression by enhancing the expression of THRSP. Mechanistically, T3 can activate tumor suppressor LKB1/AMPK/Raptor signaling as well as oncogenic PI3K/Akt signaling in HCC. Interestingly, T3-induced THRSP can augment the activation of LKB1/AMPK/Raptor signaling, yet inhibit T3-induced PI3K/Akt signaling activation, thereby preventing mTOR-induced nuclear translocation of HIF-1α, and ultimately suppressing ENO2-induced glycolysis and HCC progression. More importantly, the exogenous T3 enhances the antitumor effect of multikinase inhibitor lenvatinib in vitro and in vivo by regulating glycolysis. Our findings reveal the role and mechanism of THs in HCC progression and glucose metabolism and provide new potential therapeutic strategies for HCC treatment and drug resistance reversal.https://doi.org/10.1038/s41420-025-02378-z
spellingShingle Chun‑Cheng Yang
Yu-Chuan Yan
Guo‑Qiang Pan
Guang-Xiao Meng
Xiao Zhang
Lun-Jie Yan
Zi-Niu Ding
Dong-Xu Wang
Rui-Zhe Li
Guang-Zhen Li
Zhao‑Ru Dong
Tao Li
Thyroid hormones inhibit tumor progression and enhance the antitumor activity of lenvatinib in hepatocellular carcinoma via reprogramming glucose metabolism
Cell Death Discovery
title Thyroid hormones inhibit tumor progression and enhance the antitumor activity of lenvatinib in hepatocellular carcinoma via reprogramming glucose metabolism
title_full Thyroid hormones inhibit tumor progression and enhance the antitumor activity of lenvatinib in hepatocellular carcinoma via reprogramming glucose metabolism
title_fullStr Thyroid hormones inhibit tumor progression and enhance the antitumor activity of lenvatinib in hepatocellular carcinoma via reprogramming glucose metabolism
title_full_unstemmed Thyroid hormones inhibit tumor progression and enhance the antitumor activity of lenvatinib in hepatocellular carcinoma via reprogramming glucose metabolism
title_short Thyroid hormones inhibit tumor progression and enhance the antitumor activity of lenvatinib in hepatocellular carcinoma via reprogramming glucose metabolism
title_sort thyroid hormones inhibit tumor progression and enhance the antitumor activity of lenvatinib in hepatocellular carcinoma via reprogramming glucose metabolism
url https://doi.org/10.1038/s41420-025-02378-z
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