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Biomedical subjects

S Hama

Publications and source records attributed to S Hama.

74 records · Page 5Linked to original sources
PubMedDate not supplied

Transformation of human glioma cell lines with the p16 gene inhibits cell proliferation.

We examined the genomic status of the p16 gene in 5 human glioma cell lines by Southern blot analysis. The p16 gene was located in the 9p21 chromosomal region and homozygous deletion was detected in 4 of 5 (80%) human glioma cell lines and 5 of 15 (33%) clinical samples. We transfected the full-length human p16 gene into p16-null human glioma cell line, U251MG cells, using the plasmid vector pRc/CMV-p16 and evaluated the effect of p16 gene transfer on the growth suppression of malignant glioma cells. The transfection of p16 cDNA caused growth suppression through G1 cell cycle arrest in U251MG cells. We also examined the effect of p16 gene transfer on the chemosensitivity to cis-diamminedichloroplatinum II (CDDP), 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl) -3-nitrosourea hydrochloride (ACNU), and 5'-azacytidine (AZC). We did not detect any change in them after p16 gene transfer. These results might suggest that deletion of p16 genes promoted unrestrained growth in human glioma but has no relationship to the chemosensitivity to CDDP, ACNU and AZC.

Antineoplastic Agents↗
PubMedDate not supplied

High concentrations of recombinant adenovirus expressing p16 gene induces apoptosis in lung cancer cell lines.

In this study, we discussed the effects of treatment with recombinant adenovirus expressing p16 (AX-p16) on cell growth and cell death. Ax-p16 at 10 m.o.i. groups showed growth inhibition 3 days after gene transfection, but the cells regrew and did not undergo cell death. On the other hand, Ax-p16 at 300 m.o.i. groups showed complete cell growth inhibition leading to cell death which was apparent 7 days after p16 gene transfection. In the high m.o.i. Ax-mock groups, cell death was marked just after infection, but had diminished by 7 days after infection. Downregulation of pRB was detected only in Ax-p16 at 300 m.o.i. groups. These data suggest that a) high m.o.i. condition of Ax-p16 gives therapeutic benefits due to the combined effects of adenovirus and high expression of p16; and b) the cell killing mechanism of the p16 transgene is different from that of high m.o.i. adenoviral infection.

Adenoviruses, Human↗