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Molecular mechanisms by which cystatin-like metastasis-associated protein regulate liver metastasis of human cancer.

半胱氨酸蛋白酶抑制剂样转移相关蛋白调节人类癌症肝转移的分子机制。

基本信息

批准号：
13671311
负责人：
UTSUNOMIYA Tohru
金额：
$ 2.3万
依托单位：
Kyushu University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2001
资助国家：
日本
起止时间：
2001 至 2002
项目状态：
已结题

项目摘要

Backgrounds: We previously reported that an increased expression of cystatin-like metastasis-associated protein (CMAP) mRNA is involved in liver-specific metastasis in a mouse model. We also identified its human homologue. However, there is still no information available on the clinical significance of CMAP expression in human cancer specimens.Materials and Methods: We studied the CMAP expression levels of resected tumor and nontumor tissue specimens using a real-time quantitative reverse transcription polymerase chain reaction for 79 patients with colorectal cancer (CRC) and 65 patients with hepatocellular carcinoma (HCC). Furthermore, we identified the specific gene-expression profiles of HepG2 cells transfected with CMAP gene by cDNA microarray.Results: The mean expression level of CMAP in tumor tissue specimens was significantly higher than in the corresponding normal tissue specimens (p<0.05). A higher expression of CMAP was significantly correlated with liver metastasis (p<0.01) of CRC. The prognosis of the patients with a higher expression of CMAP was significantly worse than those with a lower expression (p=0.038). Furthermore, an increased expression of CMAP was significantly associated with intrahepatic metastasis of HCC. A cDNA microarray analysis identified 261 genes that were up-regulated and 430 genes that were down-regulated in HepG2 cells with CMAP overexpression.Conclusions: These findings imply that the expression level of CMAP in human cancer may be a new biomarker for both liver metastasis and the patient's outcome. A technique of cDNA microarray may elucidate the precise mechanisms by which increased expression of CMAP is associated with liver-specific metastasis.

背景资料：我们以前报道过胱抑素样转移相关蛋白（CMAP）mRNA表达增加参与小鼠模型的肝脏特异性转移。我们还鉴定了它的人类同源物。然而，仍然没有信息CMAP表达的临床意义，在人类cancer samples.Materials和方法：我们研究了切除的肿瘤和非肿瘤组织标本的CMAP表达水平，使用实时定量逆转录聚合酶链反应79例结直肠癌（CRC）和65例肝细胞癌（HCC）。结果：CMAP基因在肝癌组织中的平均表达水平显著高于相应的正常组织（p<0.05）; CMAP的高表达与大肠癌的肝转移密切相关（p<0.01）。CMAP高表达患者的预后显著差于低表达患者（p=0.038）。此外，CMAP表达的增加与HCC的肝内转移显著相关。cDNA微阵列分析确定了261个基因表达上调和430个基因表达下调HepG 2细胞与CMAP overexpression.Conclusions：这些研究结果表明，CMAP在人类癌症的表达水平可能是一个新的生物标志物肝转移和患者的结果。cDNA微阵列技术可以阐明CMAP表达增加与肝特异性转移相关的确切机制。