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Tumor cell alpha-N-acetylgalactosaminidase activity and its involvement in GcMAF-related macrophage activation (Abstract)

Alpha-N-acetyl galactosaminidase (alpha-NaGalase) has been reported to accumulate in serum of cancer patients and be responsible for deglycosylation of Gc protein, which is a precursor of GcMAF-mediated macrophage activation cascade, finally leading to immunosuppression in advanced cancer patients.
We studied the biochemical characterization of alpha-NaGalase from several human tumor cell lines. We also examined its effect on the potency of GcMAF to activate mouse peritoneal macrophage to produce superoxide in GcMAF-mediated macrophage activation cascade. The specific activity of alpha-NaGalases from human colon tumor cell line HCT116, human hepatoma cell line HepG2, and normal human liver cells (Chang liver cell line) were evaluated using two types of substrates; GalNAc-alpha-PNP (exo-type substrate) and Gal-beta-GalNAc-alpha-PNP (endo-type substrate).
Tumor-derived alpha-NaGalase having higher activity than normal alpha-NaGalase, had higher substrate specificity to the exo-type substrate than to the endo-type substrate, and still maintained its activity at pH 7. GcMAF enhance superoxide production in mouse macrophage, and pre-treatment of GcMAF with tumor cell lysate reduce the activity.
We conclude that tumor-derived alpha-NaGalase is different in biochemical characterization compared to normal alpha-NaGalase from normal Chang liver cells. In addition, tumor cell-derived alpha-NaGalase decreases the potency of GcMAF on macrophage activation.


Author Keywords: Alpha-N-acetylgalactosaminidase; Gal-beta-GalNAc-alpha-PNP; GalNAc-alpha-PNP; GcMAF-mediated macrophage activation cascade; Gc protein-derived macrophage activating factor (GcMAF); Mouse peritoneal macrophage; Superoxide; Tumor cells


Erratum to “Tumor cell alpha-N-acetylgalactosaminidase activity and its involvement in GcMAF-related macrophage activation”: [Comp. Biochem. Physiol. A 132 (2002) 1–8]
Comparative Biochemistry and Physiology – Part A: Molecular & Integrative PhysiologyVolume 134, Issue 2February 2003Page 481,
Saharuddin B. Mohamad, Hideko Nagasawa, Yoshihiro Uto, Hitoshi Hori
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