Lenvatinib inhibits angiogenesis and tumor fibroblast growth factor signaling pathways in human hepatocellular carcinoma models

Abstract Unresectable hepatocellular carcinoma (uHCC) is one of the most lethal and prevalent cancers worldwide, and current systemic therapeutic options for uHCC are limited. Lenvatinib, a multiple receptor tyrosine kinase inhibitor targeting vascular endothelial growth factor receptors (VEGFRs) an...

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Main Authors: Masahiro Matsuki, Taisuke Hoshi, Yuji Yamamoto, Megumi Ikemori‐Kawada, Yukinori Minoshima, Yasuhiro Funahashi, Junji Matsui
Format: Article
Language:English
Published: Wiley 2018-06-01
Series:Cancer Medicine
Subjects:
Online Access:https://doi.org/10.1002/cam4.1517
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author Masahiro Matsuki
Taisuke Hoshi
Yuji Yamamoto
Megumi Ikemori‐Kawada
Yukinori Minoshima
Yasuhiro Funahashi
Junji Matsui
author_facet Masahiro Matsuki
Taisuke Hoshi
Yuji Yamamoto
Megumi Ikemori‐Kawada
Yukinori Minoshima
Yasuhiro Funahashi
Junji Matsui
author_sort Masahiro Matsuki
collection DOAJ
description Abstract Unresectable hepatocellular carcinoma (uHCC) is one of the most lethal and prevalent cancers worldwide, and current systemic therapeutic options for uHCC are limited. Lenvatinib, a multiple receptor tyrosine kinase inhibitor targeting vascular endothelial growth factor receptors (VEGFRs) and fibroblast growth factor receptors (FGFRs), recently demonstrated a treatment effect on overall survival by statistical confirmation of noninferiority to sorafenib in a phase 3 study of uHCC. Here, we investigated mechanisms underlying the antitumor activity of lenvatinib in preclinical HCC models. In vitro proliferation assay of nine human HCC cell lines showed that lenvatinib selectively inhibited proliferation of FGF signal‐activated HCC cells including FGF19‐expressing Hep3B2.1‐7. Lenvatinib suppressed phosphorylation of FRS2, a substrate of FGFR1–4, in these cells in a concentration‐dependent manner. Lenvatinib inhibited in vivo tumor growth in Hep3B2.1‐7 and SNU‐398 xenografts and decreased phosphorylation of FRS2 and Erk1/2 within the tumor tissues. Lenvatinib also exerted antitumor activity and potently reduced tumor microvessel density in PLC/PRF/5 xenograft model and two HCC patient‐derived xenograft models. These results suggest that lenvatinib has antitumor activity consistently across diverse HCC models, and that targeting of tumor FGF signaling pathways and anti‐angiogenic activity underlies its antitumor activity against HCC tumors.
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spelling doaj-art-a133cdecf55046c4a48cc07fc66f2fed2025-08-20T03:15:04ZengWileyCancer Medicine2045-76342018-06-01762641265310.1002/cam4.1517Lenvatinib inhibits angiogenesis and tumor fibroblast growth factor signaling pathways in human hepatocellular carcinoma modelsMasahiro Matsuki0Taisuke Hoshi1Yuji Yamamoto2Megumi Ikemori‐Kawada3Yukinori Minoshima4Yasuhiro Funahashi5Junji Matsui6Tsukuba Research Laboratories Eisai Co., Ltd. Ibaraki JapanTsukuba Research Laboratories Eisai Co., Ltd. Ibaraki JapanTsukuba Research Laboratories Eisai Co., Ltd. Ibaraki JapanTsukuba Research Laboratories Eisai Co., Ltd. Ibaraki JapanTsukuba Research Laboratories Eisai Co., Ltd. Ibaraki JapanTsukuba Research Laboratories Eisai Co., Ltd. Ibaraki JapanTsukuba Research Laboratories Eisai Co., Ltd. Ibaraki JapanAbstract Unresectable hepatocellular carcinoma (uHCC) is one of the most lethal and prevalent cancers worldwide, and current systemic therapeutic options for uHCC are limited. Lenvatinib, a multiple receptor tyrosine kinase inhibitor targeting vascular endothelial growth factor receptors (VEGFRs) and fibroblast growth factor receptors (FGFRs), recently demonstrated a treatment effect on overall survival by statistical confirmation of noninferiority to sorafenib in a phase 3 study of uHCC. Here, we investigated mechanisms underlying the antitumor activity of lenvatinib in preclinical HCC models. In vitro proliferation assay of nine human HCC cell lines showed that lenvatinib selectively inhibited proliferation of FGF signal‐activated HCC cells including FGF19‐expressing Hep3B2.1‐7. Lenvatinib suppressed phosphorylation of FRS2, a substrate of FGFR1–4, in these cells in a concentration‐dependent manner. Lenvatinib inhibited in vivo tumor growth in Hep3B2.1‐7 and SNU‐398 xenografts and decreased phosphorylation of FRS2 and Erk1/2 within the tumor tissues. Lenvatinib also exerted antitumor activity and potently reduced tumor microvessel density in PLC/PRF/5 xenograft model and two HCC patient‐derived xenograft models. These results suggest that lenvatinib has antitumor activity consistently across diverse HCC models, and that targeting of tumor FGF signaling pathways and anti‐angiogenic activity underlies its antitumor activity against HCC tumors.https://doi.org/10.1002/cam4.1517angiogenesisfibroblast growth factorhepatocellular carcinomaLenvatinibvascular endothelial growth factor
spellingShingle Masahiro Matsuki
Taisuke Hoshi
Yuji Yamamoto
Megumi Ikemori‐Kawada
Yukinori Minoshima
Yasuhiro Funahashi
Junji Matsui
Lenvatinib inhibits angiogenesis and tumor fibroblast growth factor signaling pathways in human hepatocellular carcinoma models
Cancer Medicine
angiogenesis
fibroblast growth factor
hepatocellular carcinoma
Lenvatinib
vascular endothelial growth factor
title Lenvatinib inhibits angiogenesis and tumor fibroblast growth factor signaling pathways in human hepatocellular carcinoma models
title_full Lenvatinib inhibits angiogenesis and tumor fibroblast growth factor signaling pathways in human hepatocellular carcinoma models
title_fullStr Lenvatinib inhibits angiogenesis and tumor fibroblast growth factor signaling pathways in human hepatocellular carcinoma models
title_full_unstemmed Lenvatinib inhibits angiogenesis and tumor fibroblast growth factor signaling pathways in human hepatocellular carcinoma models
title_short Lenvatinib inhibits angiogenesis and tumor fibroblast growth factor signaling pathways in human hepatocellular carcinoma models
title_sort lenvatinib inhibits angiogenesis and tumor fibroblast growth factor signaling pathways in human hepatocellular carcinoma models
topic angiogenesis
fibroblast growth factor
hepatocellular carcinoma
Lenvatinib
vascular endothelial growth factor
url https://doi.org/10.1002/cam4.1517
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AT yujiyamamoto lenvatinibinhibitsangiogenesisandtumorfibroblastgrowthfactorsignalingpathwaysinhumanhepatocellularcarcinomamodels
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