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- W1591900372 abstract "Background: Although hydrogen peroxide may play an important role in the development of cancer, it can be an efficient inducer of apoptosis in cancer cells; the exact mechanism by which this action occurs is not completely understood in oral cancer cells. Method: In this study, the mechanisms by which H 2 O 2 inhibited growth and induced apoptosis were differentially investigated using HPV‐immortalized human oral keratinocytes (IHOK) and oral cancer cells (HN4). Results: H 2 O 2 treatment sensitively and dose‐dependently induced growth inhibition and typical apoptosis in IHOK and HN4 cells, as demonstrated by a decreased level of cell viability, an increased population of cells in the sub‐G 0 /G 1 phase, ladder formation of the genomic DNA, chromatin condensation and accumulation of Annexin V + /PI + cells. Furthermore, the expression of Bax, p53 and p21 WAF1/CIP1 increased, whereas the expression of Bcl‐2 decreased in immortalized and malignant keratinocytes that were treated with H 2 O 2 . In addition, cytochrome‐ c from the mitochondria was observed in H 2 O 2 ‐treated IHOK and oral cancer cells, and this was accompanied by the activation of caspase‐3 and ‐9. Additionally, H 2 O 2 treatment induced upregulation of CHOP, GRP78 and several representative endoplasmic reticulum (ER) stress‐responsive proteins, including heme oxygenase‐1. Conclusion: Overall, these results suggest that H 2 O 2 triggers apoptosis via the mitochondrial and ER stress pathway in IHOK and HN4 cells, and that increasing the cellular levels of H 2 O 2 sufficiently may lead to selective killing of oral cancer cells and therefore be therapeutically useful." @default.
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- W1591900372 date "2008-08-05" @default.
- W1591900372 modified "2023-10-17" @default.
- W1591900372 title "Endoplasmic reticulum stress is involved in hydrogen peroxide induced apoptosis in immortalized and malignant human oral keratinocytes" @default.
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- W1591900372 doi "https://doi.org/10.1111/j.1600-0714.2008.00679.x" @default.
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