Stress-induced down-regulation of tumor-associated NADH oxidase during apoptosis in transformed cells

• Published in: FEBS letters Vol. 582; no. 23-24; pp. 3445 - 3450
• Main Authors: Mao, Liang-Chi, Wang, Hsi-Ming, Lin, You-Yu, Chang, Te-Kau, Hsin, Yi-Hong, Chueh, Pin Ju
• Format: Journal Article
• Language: English
• Published: England Elsevier B.V 15.10.2008
• Subjects: Apoptosis; Apoptosis - genetics; Capsaicin; Cell Line, Tumor; Cell Proliferation; Cell Transformation, Neoplastic - genetics; Cell Transformation, Neoplastic - metabolism; Cell Transformation, Neoplastic - pathology; Down-Regulation; EGCg; Gene Knockdown Techniques; Humans; NADH, NADPH Oxidoreductases - genetics; NADH, NADPH Oxidoreductases - metabolism; Peptide Hydrolases - genetics; Peptide Hydrolases - metabolism; Stress, Physiological; Tumor-associated NADH oxidase (tNOX); Ultraviolet Rays; UVC; Tumor-associated NADH oxidase (tNOX); UVC; Capsaicin; EGCg; Down-regulation; Apoptosis
• ISSN: 0014-5793; 1873-3468
• DOI: 10.1016/j.febslet.2008.09.008

Tumor-associated NADH oxidase (tNOX) is a growth-related protein expressed in transformed cells. tNOX knockdown using RNA interference leads to a significant reduction in HeLa cell proliferation and migration, indicating an important role for tNOX in growth regulation and the cancer phenotype. Here, we show that tNOX is down-regulated during apoptosis in HCT116 cells. Treatment with diverse stresses induced a dose- and time-dependent decrease in tNOX expression that was concurrent with apoptosis. Moreover, shRNA-mediated tNOX knockdown rendered cells susceptible to apoptosis, whereas re-expression of tNOX partially recovered cell proliferation. Our results indicate that tNOX is suppressed during apoptosis and demonstrate that tNOX down-regulation sensitizes cells to stress-induced growth reduction, suggesting that tNOX is required for transformed cell growth.