NSK-01105, a Novel Sorafenib Derivative, Inhibits Human Prostate Tumor Growth Via Suppression of VEGFR2/EGFR-mediated Angiogenesis

Overview

Journal PLoS One

Specialties General Medicine
Science

Date 2015 Jan 1

PMID 25551444

Citations 6

Authors

Pengfei Yu

Liang Ye

Hongbo Wang

Guangying Du

Jianzhao Zhang

Yanhua Zuo

Jinghai Zhang

Jingwei Tian

Affiliations

Soon will be listed here.

Abstract

The purpose of this study is to investigate the anti-angiogenic activities of NSK-01105, a novel sorafenib derivative, in in vitro, ex vivo and in vivo models, and explore the potential mechanisms. NSK-01105 significantly inhibited vascular endothelial growth factor (VEGF)-induced migration and tube formation of human umbilical vein endothelial cells at non-cytotoxic concentrations as shown by wound-healing, transwell migration and endothelial cell tube formation assays, respectively. Cell viability and invasion of LNCaP and PC-3 cells were significantly inhibited by cytotoxicity assay and matrigel invasion assay. Furthermore, NSK-01105 also inhibited ex vivo angiogenesis in matrigel plug assay. Western blot analysis showed that NSK-01105 down-regulated VEGF-induced phosphorylation of VEGF receptor 2 (VEGFR2) and the activation of epidermal growth factor receptor (EGFR). Tumor volumes were significantly reduced by NSK-01105 at 60 mg/kg/day in both xenograft models. Immunohistochemical staining demonstrated a close association between inhibition of tumor growth and neovascularization. Collectively, our results suggest a role of NSK-01105 in treatment for human prostate tumors, and one of the potential mechanisms may be attributed to anti-angiogenic activities.

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