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1997 Fiscal Year Final Research Report Summary

Human GalNAc Transferase Isozyme Expression in Cancer Cells

Research Project

Project/Area Number 09044318
Research Category

Grant-in-Aid for international Scientific Research

Allocation TypeSingle-year Grants
SectionJoint Research
Research Field Gastroenterology
Research InstitutionKochi Medical School

Principal Investigator

NISHIMORI Isao  Kochi Medical School, First Department of Internal Medicine, Assistant Professor, 医学部, 助手 (30237747)

Co-Investigator(Kenkyū-buntansha) MORITA Masanori  Kochi Medical School First Department of Internal Medicine, Assistant Professor, 医学部附属病院, 助手 (30191034)
ENZAN Hideaki  Kochi Medical School, First Department of Pathology, Professor, 医学部, 教授 (00034645)
HOLLINGSWORT マイケル A.  ネブラスカ州立大学, メディカルセンター・エプリー癌研究所, 助教授
HOLLINGSWORTH Michael A.  University of Nebraska Medical Center, Eppley Cancer Institute, Associate Profes
Project Period (FY) 1997
KeywordsN-acetylgalactosamine / Glycosyltransferase / Immunohistochemistry / mRNA / Gastric cancer / Colon cancer / Breast cancer / Pancreas cancer
Research Abstract

1.Polyclonal antibodies against two isozymes of the human UDP-N-acetylgalactosamine : polypeptide N-acetylgalactosaminyltransferase (T1 and T2) were produced by immunizations of rabbits with synthetic peptides. Histological expression and localization of T1 and T2 in normal and cancer colon tissues were studied by immunohistochmical analysis with these antibodies. In cancer tissuses, T1 and T2 expressions were observed in 1 (8%) and 9 (69%) out of 13 patients with colon cancer, respectively. In normal counterpart of colon tissues in 6 patients with colon cancer and in normal colon tissues in 20 subjects, neither T1 nor T2 expression was observed. These results showed the heterogeneous and up-regulated expression of T2 protein during carcinogenesis of colon epithelial cells.
The levels of mRNA expression of three UDP-N-acetylgalactosamine : polypeptide N-acetylgalactosaminyltransferase (T1, T2, and T3) were quantified for human adenocarcinoma cell lines from pancreas, colon, stomach, and breast. T1 and T2 were expressed constitutively and at low levels in most or all cell lines examined. T3 was differentially expressed. Well-differentiated adenocarcinoma cell lines expressed high levels and moderately differetiated cell lines expressed lower levels of T3. Cell lines classified as poorly differentiated failed to express T3 mRNA at levels that could be detected by Northern blot analysis. Differential expression of the T3 protein was confirmed in these cell lines by Western blotting. We propose that glycosylation in tumor cell lines may be regulated in part by differential expression of UDP-N-acetylgalactosamine : polypeptide N-acetylgalactosaminyltransferase.

  • Research Products

    (4 results)

All Other

All Publications (4 results)

  • [Publications] Sutherlin,ME: "Expression of three UDP-N-acetyl-α-D-galactosamine:polypeptide GalNAc N-acetylgalactosaminyltransferases in adenocarcinoma cell lines." Cancer Research. 57. 4744-4748 (1997)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Adachi,T: "Increased sensitivity of gastric cancer cells to natural killer and lymphokine-activated killer cells by antisense suppression of N-acetylgalactosaminyltransferase." Journal of Immunology. 159. 2645-2651 (1997)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Sutherlin ME,Nishimori I,Caffrey T,Bennett EP,Hassan H,Mandel U,Mack D,Iwamura T,Clausen H,Hollingsworth MA: "Expression of three UDP-N-acetyl-alpha-D-galactosamine : polypeptide GalNAc N-acetylgalactosaminyltransferases in adenocarcinoma cell lines." Cancer Research. 57. 4744-4748 (1997)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Adachi T,Hinoda Y,Nishimori I,Adachi M,Imai K: "Increased sensitivity of gastric cancer cells to natural killer and lymphokine-activated killer cells by antisense suppression of N-acetylgalactosaminyltransferase." Journal of Immunology. 159. 2645-2651 (1997)

    • Description
      「研究成果報告書概要(欧文)」より

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Published: 1999-03-16  

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