Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Hama, S. et al.

Adenovirus-mediated p16 gene transfer prevents drug- induced cell death through G1 arrest in human glioma cells.

This study examined the effects of full-length p16 gene transfer by recombinant adenovirus on cell growth and on sensitivity to CDDP or ACNU chemotherapies. We developed a recombinant adenovirus expressing the full-length human p16 gene (AxCA-hp16) by the COS-TPC method. AxCA-hp16 was infected into the p16-null human glioma cell line, U251MG. AxCA-hp16 infection inhibited proliferation of U251MG cells. A proliferation assay employing MTT showed that AxCA-hp16 infection induced chemoresistance, preventing CDDP-induced cell death (11- to 15-fold) and ACNU-induced cell death (80- to 92-fold). In the absence of AxCA-hp16, cell death was induced with CDDP or ACNU at 3 to 5 days after treatment, as demonstrated by Trypan-blue exclusion. Flow-cytometric analysis showed that CDDP or ACNU arrested cells in the G2 phase on day 1 and that cells re-entered the cycle on day 3. However, the cells infected with AxCA-hp16 after CDDP or ACNU treatment showed G1 arrest on day 5 after re-entering the cycle from G2 arrest on day 3. The cells infected with AxCA-hp16 before CDDP or ACNU treatment showed G1 arrest over the 5 days after the infection. This study demonstrated that G1 arrest induced with p16-gene expression prevents ACNU- or CDDP-induced cell death. The cell death induced by ACNU and CDDP therefore appears to occur in the phase after the G1/S check point.[1]

References

Adenovirus-mediated p16 gene transfer prevents drug-induced cell death through G1 arrest in human glioma cells. Hama, S., Heike, Y., Naruse, I., Takahashi, M., Yoshioka, H., Arita, K., Kurisu, K., Goldman, C.K., Curiel, D.T., Saijo, N. Int. J. Cancer (1998) [Pubmed]

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