Overexpression of the MTA1 gene in gastrointestinal carcinomas: Correlation with invasion and metastasis

Yasushi Toh, Eiji Oki, Shinya Oda, Eriko Tokunaga, Shinji Ohno, Yoshihiko Maehara, Garth L. Nicolson, Keizo Sugimachi

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163 Citations (Scopus)


The total gene is a recently identified novel candidate metastasis- associated gene. The deduced amino acid sequence contains an src homology-3 domain binding motif, a zinc finger motif and possible phosphorylation sites, suggesting that this gene is involved in signal transduction or regulation of gene expression. The purpose of our study was to examine the mRNA expression levels of the MTAI, the human homologue of the rat mta1 gene in colorectal and gastric carcinomas and thus to evaluate the relevance of the expression of this gene to human carcinoma progression. The expression of MTAI mRNA in 36 colorectal and 34 gastric carcinoma samples was compared with that in corresponding normal mucosa tissues by semi-quantitative reverse- transcription polymerase chain reaction (RT-PCR) and the results were compared with clinicopathologic data. A relative overexpression of MTAI mRNA (tumor/normal ratio ≤2) was observed in 14 of 36 (38.9%) colorectal carcinomas and 13 of 34 (38.2%) gastric carcinomas. Clinicopathologic correlations demonstrated that in colorectal carcinomas, tumors overexpressing MTAI mRNA exhibited a significantly deeper wall invasion and a higher rate of metastasis to lymph nodes, and tended to be at an advanced Dukes' stage with frequent lymphatic involvement. In gastric carcinomas, the tumors overexpressing MTAI mRNA showed significantly higher rates of serosal invasion and lymph node metastasis and tended to have a higher rate of vascular involvement. Our data suggest that overexpression of the MTAI gene correlates with tumor invasion and the presence of metastases and that a high expression of MTAI mRNA may be a potential indicator for assessing the malignant potential of colorectal and gastric carcinomas.

Original languageEnglish
Pages (from-to)459-463
Number of pages5
JournalInternational Journal of Cancer
Issue number4
Publication statusPublished - 1997

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research


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