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首页> 外文期刊>Pathobiology: journal of immunopathology, molecular and cellular biology >Induction of hRAD9 Is Required for G2/M Checkpoint Signal Transduction in Gastric Cancer Cells.
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Induction of hRAD9 Is Required for G2/M Checkpoint Signal Transduction in Gastric Cancer Cells.

机译：胃癌细胞中G2 / M检查点信号转导需要hRAD9的诱导。

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摘要

DNA damage triggers the activation of checkpoints that delay cell cycle progression to allow for DNA repair. Loss of G2 checkpoints provides a growth advantage for tumor cells undergoing aberrant mitosis. However, the precise mechanisms of G2 checkpoints acting in gastric cancer are unknown. Here, we analyzed the G2 checkpoint function in two gastric cancer cells, MKN-28 cells containing a mutant p53 gene and MKN-45 cells which have wild-type p53. Two agents damaging DNA, camptothecin (CPT) or ultraviolet light (UV), were utilized to trigger a G2 phase cell cycle checkpoint response in these tumor cells. Both CPT and UV inhibited the growth of MKN-45 cells, whereas they did not affect the growth of MKN-28 cells. CPT induced cell cycle arrest at the G2/M phase and enhanced the expression of human RAD9 (hRAD9) in MKN-45 cells. In addition, hRAD9 showed perinuclear staining and similar localization with Bcl-2 in MKN-45 cells but not in MKN-28 cells after having applied CPT or UV light. These results suggest that besides p53 activity, the induction of hRAD9 is required for G2/M checkpoint signal transduction in gastric cancer cells.
机译：DNA损伤会触发检查点的激活，从而延缓细胞周期进程，从而允许DNA修复。 G2检查点的丢失为经历异常有丝分裂的肿瘤细胞提供了生长优势。但是，尚不清楚G2检查点在胃癌中起作用的确切机制。在这里，我们分析了两种胃癌细胞中的G2检查点功能，这两种胃癌细胞含有突变型p53基因，而MKN-45细胞则具有野生型p53。喜树碱（CPT）或紫外线（UV）这两种破坏DNA的药物被用来触发这些肿瘤细胞中的G2期细胞周期检查点反应。 CPT和紫外线都抑制MKN-45细胞的生长，而它们不影响MKN-28细胞的生长。 CPT诱导细胞周期阻滞在G2 / M期，并增强MKN-45细胞中人RAD9（hRAD9）的表达。此外，hRAD9在施加CPT或紫外线后，在MKN-45细胞中显示出核周染色和类似的Bcl-2定位，而在MKN-28细胞中没有显示。这些结果表明，除了p53活性，胃癌细胞中G2 / M检查点信号转导还需要诱导hRAD9。

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