Rosiglitazone suppresses gastric carcinogenesis by up-regulating HCaRG expression
Rosiglitazone suppresses gastric carcinogenesis by up-regulating HCaRG expression
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DOI：
10.3892/or_00000114
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发表时间：
2008-11-01
期刊：
影响因子：
4.2
通讯作者：
Leung, Wai K.
中科院分区：
文献类型：
--
作者：
Chen, Bai-Li;Yu, Jun;Leung, Wai K.
我们以前的研究表明，PPAR γ配体罗格列酮预防化学致癌物N-甲基-N'-硝基-N-亚硝基胍（MNNG）诱导的大鼠胃癌发生。在这项研究中，我们试图确定新的罗格列酮的抗癌机制。通过使用Uniset Rat I Bioarray微阵列检测MNNG诱导和罗格列酮治疗的胃癌的基因表达谱，我们确定了一个在罗格列酮治疗组中表现出显著反应的基因。与MNNG组相比，罗格列酮治疗组的高血压相关钙调节基因（HCaRG）在大鼠胃癌中显著上调。我们进一步检测了HCaRG在人胃癌组织中的表达，发现HCaRG在人胃癌组织中的表达下调。罗格列酮可明显诱导AGS细胞系HCaRG的表达。HCaRG表达上调可能是罗格列酮化学预防胃癌的机制之一。
Our previous study demonstrated that PPAR gamma ligand rosiglitazone prevents gastric carcinogenesis in rats induced by chemical carcinogen N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). In this study, we attempted to identify novel anticancer mechanisms of rosiglitazone. By examining the gene expression profiles of MNNG-induced and rosiglitazone-treated gastric cancer with Uniset Rat I Bioarray microarray, we identified a gene that showed prominent responses in the rosiglitazone-treated group. The hypertension-related, calcium-regulated gene (HCaRG) was significantly up-regulated in rat gastric carcinoma of the rosiglitazone-treated group when compared with the MNNG group. We further examined HCaRG expression in human gastric cancer and found that the expression of HCaRG was down-regulated in human gastric cancerous tissue. Rosiglitazone markedly induced the expression of HCaRG in the AGS cell line. The up-regulation of HCaRG may be one of the mechanisms underlying the chemopreventive effect of rosiglitazone in gastric cancer.