2002 Fiscal Year Final Research Report Summary
Molecular mechanisms by which cystatin-like metastasis-associated protein regulate liver metastasis of human cancer.
| Project/Area Number |
13671311
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | Kyushu University |
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Principal Investigator |
UTSUNOMIYA Tohru Medical Institute of Bioregulation Kyushu Univ. lecturer, 生体防御医学研究所, 講師 (30304801)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHITAKE Shinichirou Medical Institute of Bioregulation Kyushu Univ. Research Associate, 生体防御医学研究所, 助手 (80315142)
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| Project Period (FY) |
2001 – 2002
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| Keywords | Cystatin / Colorectal cancer / Hepatocellular carcinoma / Liver metastasis / Protease inhibitor / Gene transfection / DNA microarray |
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| Research Abstract |
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.
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Research Products
(20 results)
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[Publications] Mimori K, Shiraishi T, Mashino K, Yoshinaga K, Masuda T, Yamashita K, Utsunomiya T, Barnard GF, Alonso MA, Inoue H, Mori M:: "MAL gene reexpression in esophageal cancer suppresses motility, invasion and tumorigenicity and enhances apoptosis through the Fas pathway."Oncogene. (in press).
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