Cutaneous squamous cell carcinoma (SCC) is a common cancer that significantly decreases the quality of life. It is known that\nexternal stimulus such as ultraviolet (UV) radiation induces cutaneous SCC via provoking oxidative stress. NAD(P)H dehydrogenase\n1 (NQO1) is a ubiquitous flavoenzyme that functions as a guardian against oxidative stress. However, the effect of\nNQO1 on cutaneous SCC is not clearly elucidated. In this study, we investigated the effect of NQO1 on cutaneous SCC cells using\nthe recombinant adenoviruses that can upregulate and/or downregulate NQO1 expression. Overexpression of NQO1 resulted in\nsignificant decrease of cell proliferation and colony forming activity of SCC lines (SCC12 and SCC13 cells). By contrast,\nknockdown of NQO1 increased the cell proliferation and colony forming activity. Accordingly, the levels of proliferation-related\nregulators, such as Cyclin D1, Cyclin E, PCNA, SOX2, and p63, were decreased by the overexpression of NQO1, while those were\nincreased by knockdown of NQO1. In addition, NQO1 affected the invasion and migration of SCC cells in a very similar way, with\nthe regulation of epithelial-mesenchymal transition- (EMT-) related molecules, including E-cadherin, N-cadherin, Vimentin,\nSnail, and Slug. Finally, the overexpression of NQO1 decreased the level of phosphorylated AKT, JNK, and p38 MAPK, while the\nknockdown of NQO1 increased the level of phosphorylated signaling molecules. Based on these data, NQO1 has tumor suppressive\nfunction in cutaneous SCC cells.
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