The A3 adenosine receptor agonist CF102 induces apoptosis of hepatocellular carcinoma via de-regulation of the Wnt and NF-κB signal transduction pathways

被引：131

作者：

Bar-Yehuda, S. ^{[1
]}

Stemmer, S. M. ^{[2
]}

Madi, L. ^{[1
]}

Castel, D. ^{[1
]}

Ochaion, A. ^{[1
]}

Cohen, S. ^{[1
]}

Barer, F. ^{[1
]}

Zabutti, A. ^{[1
]}

Perez-Liz, G. ^{[3
]}

Del Valle, L. ^{[3
]}

Fishman, P. ^{[1
]}

机构：

[1] Can Fite BioPharma Ltd, Kiryat Matalon, Israel

[2] Tel Aviv Univ, Sackler Sch Med, Rabin Med Ctr, Davidoff Ctr,Inst Oncol, IL-49100 Petah Tiqwa, Israel

[3] Temple Univ, Sch Med, Neuropathol Core & Ctr Neurovirol, Dept Neurosci, Philadelphia, PA 19122 USA

来源：

INTERNATIONAL JOURNAL OF ONCOLOGY | 2008年 / 33卷 / 02期

关键词：

A(3) adenosine receptor; HCC; CF102; NF-kappa B; Wnt; apoptosis;

D O I：

10.3892/ijo_00000008

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The A(3) adenosine receptor (A(3)AR) is highly expressed in tumors and was suggested as a target for cancer treatment. In this study, we show that A(3)AR is highly expressed in tumor tissues and in peripheral blood mononuclear cells (PBMCs) derived from patients with HCC, as well as from HCC tumor-bearing rats. The high expression level of the receptor was directly correlated to overexpression of NF-kappa B, known as a transcription factor of A(3)AR. CF102, a synthetic highly selective agonist to A3AR induced a marked dose response inhibition of tumor growth in N1S1 HCC tumor rats, via de-regulation of the NF-kappa B and the Wnt signal transduction pathways, resulting in apoptosis of tumor cells. Taken together, A(3)AR is highly expressed in tumors and PBMCs of HCC patients and tumor-bearing rats. CF102 induced apoptosis and tumor growth inhibition. These data suggest A(3)AR as a novel targeted therapy to treat HCC.

引用

页码：287 / 295

页数：9

共 39 条

[1] Nuclear factor-κB and liver carcinogenesis [J].