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Matthew EM, Yen TJ, Dicker DT, Dorsey JF, Yang WS, Navaraj A, El-Deiry WS
Replication stress, defective S-phase checkpoint and increased death in Plk2-deficient human cancer cells
Cell Cycle (2007) 6:2571-2578.
We previously reported that the Polo-like kinase 2 gene (Plk2/Snk) is a direct target for transcriptional regulation by p53 and that silencing Plk2 sensitizes cancer cells to Taxol-induced apoptosis. Our goals have been to better understand why Plk2 is regulated by p53 and how Plk2 signals protection from cell death through checkpoint activation. We found that following knock-down of Plk2 in wild-type p53 expressing H460 human non-small cell lung cancer cells there was a significant increase in cell death observed in aphidicolin-treated cells and a further increase after release from aphidicolin- block. The highest levels of cell death were observed when Plk2-deficient cells were released from both aphidicolin and etoposide treatment. These results suggested that a defective S-phase checkpoint may contribute to enhanced sensitivity of Plk2-deficient cells to replication stress. Consistent with this hypothesis, we observed higher levels of Serine 139 H2AX phosphorylation i!
Publication Date: 2007-10-01.
Last updated on Saturday, August 22, 2020