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Expression of the smg p25A (a ras p21-like GTP-binding Protein) Gene in Human Neuroblastoma Cell Lines and Tumor Tissues¹

Departments of Pediatrics [K. S., H. N.] and Biochemistry [Y. T.], Kobe University School of Medicine, Kobe, 650, Japan; Division of Hematology and Oncology, Hyogo Prefectural Children's Hospital, Kobe, 654, Japan [S. M.]; Department of Pediatrics, National Kure Hospital, Kure, 737, Japan [T. T.]; and Department of Pediatric Surgery, Faculty of Medicine, Kyushu University, Fukuoka, 812, Japan [A. N.]

We have examined expression of the smg p25A (a ras p21-like GTP-binding protein) gene in neural crest-derived tumor cell lines and neuroblastoma tissues. The human neuroblastoma cell lines GOTO, IMR-32, NB-1, and SK-N-SH expressed the 1.6-kilobase smg-25A mRNA. SH-SY5Y and SH-IN, variant cell lines with a neuronal phenotype derived from SK-N-SH, expressed much more smg-25A mRNA than did SH-EP1, a variant line with an epithelium-like phenotype also derived from SK-N-SH. The primitive neuroectodermal tumor cell lines SK-N-MC and KU-SN and the Ewing's sarcoma cell lines RD-ES and SK-ES expressed the smg-25A mRNA to a much smaller extent than did neuroblastoma cell lines. Of 15 human neuroblastoma specimens tested, 13 expressed the smg-25A mRNA to various extents. When the relative ratio of the smg-25A mRNA level to the glyceraldehyde-3-phosphate dehydrogenase mRNA level was compared among neuroblastoma tumor tissues, the value was significantly higher in tumors histologically diagnosed as ganglioneuroblastoma. The smg-25A mRNA was not detected in the tissues of Hodgkin's lymphoma, Wilms' tumor, Ewing's sarcoma, or undifferentiated sarcoma of the liver. These results suggest that the smg-25A mRNA level is closely related to the neuronal differentiation state of tumors derived from the neural crest.

¹ The investigation in the Department of Pediatrics was supported by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science, and Culture, Japan (1989), a Grant-in-Aid for Research on Mental Diseases from the Ministry of Health and Welfare, Japan (1989), and a grant from Natio Foundation. The investigation in the Department of Biochemistry was supported by Grants-in-Aid for Scientific Research and Cancer Research from the Ministry of Education, Science, and Culture, Japan (1989), Grants-in-Aid for Abnormalities in Hormone Receptor Mechanisms (1989), Cardiovascular Diseases (1989), and Cancer Research (1989) from the Ministry of Health and Welfare, Japan, and by grants from the Yamanouchi Foundation for Research on Metabolic Disease (1989) and the Research Program on Cell Calcium Signal in the Cardiovascular System (1989).

² To whom requests for reprints should be addressed, at Department of Pediatrics, Kobe University School of Medicine, Kobe, 650, Japan.

Received 5/25/90. Accepted 8/20/90.

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