Dataset Information


Differentially expressed genes in H2AX knockdown cells undergoing apoptosis

ABSTRACT: H2AX has been characterized as a novel tumor suppressor protein. Difficiency of H2AX will result in apoptotic inhibition of cancer cells. However, how H2AX epigenetically regulates apoptosis of cancer cells is still unclear. To reveal the genes expression regulated by H2AX and involved in apoptosis, the microarray profiling analysis was employed to identify differentially expressed genes in H2AX knockdown lung cancer cells and control ones after apoptotic induction. H2AX was knockdown by miRNA interfering system in human lung cancer originated cell A549 and the stable cell line named P1, while the control stable cell line named C. Genes with greater than 1.2-fold change and P-value <0.05 were identified as differentially expressed genes between C and P1 cells both with apoptosis induction. The two groups including control (C) and H2AX knockdown lung cancer cells (P1) were harvested 48 h after VP-16 treatment. Three independent experiments were performed for each group.


ORGANISM(S): Homo sapiens  

SUBMITTER: Chengrong Lu  

PROVIDER: E-GEOD-43498 | ArrayExpress | 2013-01-16



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Genome-wide transcriptional analysis of apoptosis-related genes and pathways regulated by H2AX in lung cancer A549 cells.

Lu Chengrong C   Xiong Min M   Luo Yuan Y   Li Jing J   Zhang Yanjun Y   Dong Yaqiong Y   Zhu Yanjun Y   Niu Tianhui T   Wang Zhe Z   Duan Lianning L  

Apoptosis : an international journal on programmed cell death 20130901 9

Histone H2AX is a novel tumor suppressor protein and plays an important role in apoptosis of cancer cells. However, the role of H2AX in lung cancer cells is unclear. The detailed mechanism and epigenetic regulation by H2AX remain elusive in cancer cells. We showed that H2AX was involved in apoptosis of lung cancer A549 cells as in other tumor cells. Knockdown of H2AX strongly suppressed apoptosis of A549 cells. We clarified the molecular mechanisms of apoptosis regulated by H2AX based on genome-  ...[more]

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