Abstract.A tumor-associated antigen RCAS1 (receptor binding cancer antigen expressed on SiSo cells) induces cell cycle arrest and apoptosis to a putative RCAS1 receptor (RCAS1-R) expressing cells such as T, B, and natural killer cells. Its expression is related with clinical poor prognosis of some malignant tumors. It is suggested that the expression of RCAS1 in tumor cells plays an important role in evasion from host immune system resulting tumor progression, invasion and metastasis. However, the mechanism of RCAS1 induced cell cycle arrest and apoptosis has not been clarified. In this study, we established a mouse L cell line transformed with tetracycline-induced rcas1 gene expression system and analyzed the RCAS1 functions. We showed that RCAS1 induced cytochrome c release and activation of caspase-3 for apoptosis. Moreover, we investigated cell cycle associated proteins and revealed that cyclin D3 decreased significantly and no change was seen in the expression levels of the other proteins. These results suggest that cyclin D3 is one of the key target molecules in the RCAS1-RCAS1-R signaling pathway.
Alkaline phosphatase (ALPase) and Mg2+-activated ATPase (Mg2+-ATPase) activities were demonstrated in human brain tumors by light and electron microscopy. Four cases of glioma, i.e., two cases of astrocytoma, grade II, and two cases of glioblastoma, were used as materials. At the light microscopic level, Mg2+-ATPase activity was observed in the capillary wall and glial cells of both astrocytoma and glioblastoma. ALPase activity was restricted to the capillary wall. Its activity was stronger in glioblastoma than in astrocytoma. By electron microscopy, in astrocytoma, reaction product representing Mg2+-ATPase activity was distributed in the plasma membranes of endothelial cells and pericytes. Activity was primarily localized at the abluminal surface of endothelial cells and the surface of pericytes facing endothelium. The plasma membrane of glial cells was also positive. ALPase activity revealed essentially the same distribution pattern in blood vessels as above. In glioblastoma, on the other hand, activities of both phosphatases were markedly positive on the luminal surface of the plasma membrane of endothelial cells. They were much stronger than those along the abluminal endothelial surface. Phosphatase activities in brain tumor appear to change in localization pattern in association with glioma malignancy. This might reflect a functional aspect of changes in blood-brain barrier in glioma.
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