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Current Cancer Drug Targets

Editor-in-Chief

ISSN (Print): 1568-0096
ISSN (Online): 1873-5576

Sunitinib (SUTENT, SU11248) Suppresses Tumor Growth and Induces Apoptosis in Xenograft Models of Human Hepatocellular Carcinoma

Author(s): H. Huynh, V. C. Ngo, S. P. Choo, D. Poon, H. N. Koong, C. H. Thng, H. C. Toh, L. Zheng, L. C. Ong, Y. Jin, I. C. Song, A. P.C. Chang, H. S. Ong, A. Y.F. Chung, P. K.H. Chow and K. C. Soo

Volume 9, Issue 6, 2009

Page: [738 - 747] Pages: 10

DOI: 10.2174/156800909789271530

Price: $65

Abstract

Hepatocellular carcinoma (HCC) is the fifth most common and third deadliest primary neoplasm. Since HCC is a particularly vascular solid tumor, we determined the antitumor and antiangiogenic activities of sunitinib malate, a potent inhibitor of two receptors involved in angiogenesis – vascular endothelial growth factor receptor (VEGFR) and plateletderived growth factor receptor (PDGFR). In the present study, we reported that treatment of HepG2 and SK-Hep-1 cells with sunitinib led to growth inhibition and apoptosis in a dose-dependent fashion. Sunitinib inhibited phosphorylation of VEGFR-2 at Tyr951 and PDGFR-β at Tyr1021 both in vitro and in vivo. Sunitinib also suppressed tumor growth of five patient-derived xenografts. Sunitinib-induced tumor growth inhibition was associated with increased apoptosis, reduced microvessel density and inhibition of cell proliferation. This study provides a strong rationale for further clinical investigation of sunitinib in patients with hepatocellular carcinoma.

Keywords: Sunitinib, hepatocellular carcinoma, growth inhibition, anti-angiogenesis


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