RIP1 potentiates BPDE-induced transformation in human bronchial epithelial cells through catalase-mediated suppression of excessive reactive oxygen species

Carcinogenesis

Volumn 34, Issue 9, 2013, Pages 2119-2128

  Wang, Qiong ^a,b   Chen, Wenshu ^b   Xu, Xiuling ^b   Li, Bilan ^b   He, Weiyang ^b   Padilla, Mabel T ^b   Jang, Jun Ho ^b,c   Nyunoya, Toru ^b,c   Amin, Shantu ^d   Wang, Xia ^a   Lin, Yong ^b  

^a SICHUAN UNIVERSITY   (China)

^b LOVELACE RESPIRATORY RESEARCH INSTITUTE   (United States)

^c NEW MEXICO VA HEALTH CARE SYSTEM   (United States)

^d PENN STATE COLLEGE OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CATALASE; CIGARETTE SMOKE; DIHYDROXYBENZO[A]PYRENE OXIDE; MITOGEN ACTIVATED PROTEIN KINASE; MITOGEN ACTIVATED PROTEIN KINASE P38; REACTIVE OXYGEN METABOLITE; RECEPTOR INTERACTING PROTEIN 1; RECEPTOR PROTEIN; STRESS ACTIVATED PROTEIN KINASE; SYNAPTOPHYSIN; UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BRONCHIAL EPITHELIAL CELL; BRONCHUS MUCOSA; CARCINOGENESIS; CELL DEATH; CELL SURVIVAL; CELL TRANSFORMATION; CONTROLLED STUDY; CYTOTOXICITY; DNA DAMAGE; ENZYME ACTIVITY; ENZYME DEGRADATION; ENZYME REPRESSION; EPITHELIUM CELL; GENE SILENCING; HUMAN; HUMAN CELL; HUMAN TISSUE; LUNG NON SMALL CELL CANCER; MALIGNANT TRANSFORMATION; MOUSE; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN FUNCTION; SMOKING;

ANIMALS; BRONCHI; CATALASE; CELL SURVIVAL; DNA DAMAGE; EPITHELIAL CELLS; GENE EXPRESSION REGULATION, NEOPLASTIC; HUMANS; LUNG NEOPLASMS; MICE; NUCLEAR PORE COMPLEX PROTEINS; OXIDATIVE STRESS; REACTIVE OXYGEN SPECIES; RNA-BINDING PROTEINS; SMOKING;

EID: 84886994137     PISSN: 01433334     EISSN: 14602180     Source Type: Journal    
DOI: 10.1093/carcin/bgt143     Document Type: Article

References (49)

1. Hanahan, D. et al. (2011) Hallmarks of cancer: the next generation. Cell, 144, 646-674.
2. Festjens, N. et al. (2007) RIP1, a kinase on the crossroads of a cell's decision to live or die. Cell Death Differ., 14, 400-410.
3. Meylan, E. et al. (2004) RIP1 is an essential mediator of Toll-like receptor 3-induced NF-kappa B activation. Nat. Immunol., 5, 503-507.
4. Zhang, J. et al. (2011) RIP1-mediated regulation of lymphocyte survival and death responses. Immunol. Res., 51, 227-236.
5. Kelliher, M.A. et al. (1998) The death domain kinase RIP mediates the TNF-induced NF-kappaB signal. Immunity, 8, 297-303.
6. Ting, A.T. et al. (1996) RIP mediates tumor necrosis factor receptor 1 activation of NF-kappaB but not Fas/APO-1-initiated apoptosis. EMBO J., 15, 6189-6196.
7. Lin, Y. et al. (2000) The death domain kinase RIP is essential for TRAIL (Apo2L)-induced activation of IkappaB kinase and c-Jun N-terminal kinase. Mol. Cell. Biol., 20, 6638-6645.
8. Kaiser, W.J. et al. (2005) Apoptosis induced by the toll-like receptor adaptor TRIF is dependent on its receptor interacting protein homotypic interaction motif. J. Immunol., 174, 4942-4952.
9. Meylan, E. et al. (2005) The RIP kinases: crucial integrators of cellular stress. Trends Biochem. Sci., 30, 151-159.
10. Hur, G.M. et al. (2003) The death domain kinase RIP has an essential role in DNA damage-induced NF-kappa B activation. Genes Dev., 17, 873-882.
11. Park, J. et al. (2012) ARD1 binding to RIP1 mediates doxorubicin-induced NF-?B activation. Biochem. Biophys. Res. Commun., 422, 291-297.
12. Bai, L. et al. (2011) Blocking NF-KB and Akt by Hsp90 inhibition sensitizes Smac mimetic compound 3-induced extrinsic apoptosis pathway and results in synergistic cancer cell death. Apoptosis, 16, 45-54.
13. Palacios, C. et al. (2010) Down-regulation of RIP expression by 17-dimethylaminoethylamino- 17-demethoxygeldanamycin promotes TRAILinduced apoptosis in breast tumor cells. Cancer Lett., 287, 207-215.
14. Wang, X. et al. (2006) 17-Allylamino-17-demethoxygeldanamycin synergistically potentiates tumor necrosis factor-induced lung cancer cell death by blocking the nuclear factor-kappaB pathway. Cancer Res., 66, 1089-1095.
15. Wang, L. et al. (2008) TNF-alpha induces two distinct caspase-8 activation pathways. Cell, 133, 693-703.
16. Holler, N. et al. (2000) Fas triggers an alternative, caspase-8-independent cell death pathway using the kinase RIP as effector molecule. Nat. Immunol., 1, 489-495.
17. Lin, Y. et al. (2004) Tumor necrosis factor-induced nonapoptotic cell death requires receptor-interacting protein-mediated cellular reactive oxygen species accumulation. J. Biol. Chem., 279, 10822-10828.
18. Tenev, T. et al. (2011) The Ripoptosome, a signaling platform that assembles in response to genotoxic stress and loss of IAPs. Mol. Cell, 43, 432-448.
19. Devin, A. et al. (2003) The role of the death-domain kinase RIP in tumournecrosis- factor-induced activation of mitogen-activated protein kinases. EMBO Rep., 4, 623-627.
20. Ventura, J.J. et al. (2004) JNK potentiates TNF-stimulated necrosis by increasing the production of cytotoxic reactive oxygen species. Genes Dev., 18, 2905-2915.
21. Lee, T.H. et al. (2003) The death domain kinase RIP1 is essential for tumor necrosis factor alpha signaling to p38 mitogen-activated protein kinase. Mol. Cell. Biol., 23, 8377-8385.
22. Lin, Y. et al. (1999) Cleavage of the death domain kinase RIP by caspase-8 prompts TNF-induced apoptosis. Genes Dev., 13, 2514-2526.
23. Darding, M. et al. (2012) IAPs: guardians of RIPK1. Cell Death Differ., 19, 58-66.
24. O'Donnell, M.A. et al. (2011) RIP1 comes back to life as a cell death regulator in TNFR1 signaling. FEBS J., 278, 877-887.
25. Park, S. et al. (2009) The receptor interacting protein 1 inhibits p53 induction through NF-kappaB activation and confers a worse prognosis in glioblastoma. Cancer Res., 69, 2809-2816.
26. Park, S. et al. (2009) RIP1 activates PI3K-Akt via a dual mechanism involving NF-kappaB-mediated inhibition of the mTOR-S6K-IRS1 negative feedback loop and down-regulation of PTEN. Cancer Res., 69, 4107-4111.
27. Guza, R. et al. (2011) Influence of C-5 substituted cytosine and related nucleoside analogs on the formation of benzo[a]pyrene diol epoxide-dG adducts at CG base pairs of DNA. Nucleic Acids Res., 39, 3988-4006.
28. Ding, J. et al. (2006) Effects of polycyclic aromatic hydrocarbons (PAHs) on vascular endothelial growth factor induction through phosphatidylinositol 3-kinase/AP-1-dependent, HIF-1alpha-independent pathway. J. Biol. Chem., 281, 9093-9100.
29. Ramirez, R.D. et al. (2004) Immortalization of human bronchial epithelial cells in the absence of viral oncoproteins. Cancer Res., 64, 9027-9034.
30. Wang, X. et al. (2007) Sensitization of TNF-induced cytotoxicity in lung cancer cells by concurrent suppression of the NF-kappaB and Akt pathways. Biochem. Biophys. Res. Commun., 355, 807-812.
31. Ju, W. et al. (2007) A critical role of luteolin-induced reactive oxygen species in blockage of tumor necrosis factor-activated nuclear factorkappaB pathway and sensitization of apoptosis in lung cancer cells. Mol. Pharmacol., 71, 1381-1388.
32. Damiani, L.A. et al. (2008) Carcinogen-induced gene promoter hypermethylation is mediated by DNMT1 and causal for transformation of immortalized bronchial epithelial cells. Cancer Res., 68, 9005-9014.
33. Xu, X. et al. (2012) MUC1 contributes to BPDE-induced human bronchial epithelial cell transformation through facilitating EGFR activation. PLoS One, 7, e33846.
34. Nyunoya, T. et al. (2011) Antioxidant diet protects against emphysema, but increases mortality in cigarette smoke-exposed mice. COPD, 8, 362-368.
35. Jablonska, E. et al. (2010) Transforming growth factor-ß1 induces expression of human coagulation factor XII via Smad3 and JNK signaling pathways in human lung fibroblasts. J. Biol. Chem., 285, 11638-11651.
36. Karahashi, H. et al. (2009) Lipopolysaccharide-induced apoptosis in transformed bovine brain endothelial cells and human dermal microvessel endothelial cells: the role of JNK. J. Immunol., 182, 7280-7286.
37. Makeeva, N. et al. (2007) Role of TAB1 in nitric oxide-induced p38 activation in insulin-producing cells. Int. J. Biol. Sci., 3, 71-76.
38. Li, Z. et al. (2011) Epidermal growth factor receptor-mediated tissue transglutaminase overexpression couples acquired tumor necrosis factor- related apoptosis-inducing ligand resistance and migration through c-FLIP and MMP-9 proteins in lung cancer cells. J. Biol. Chem., 286, 21164-21172.
39. Gao, D. et al. (2005) Benzo[a]pyrene and its metabolites combined with ultraviolet A synergistically induce 8-hydroxy-2'-deoxyguanosine via reactive oxygen species. Free Radic. Biol. Med., 39, 1177-1183.
40. Nimnual, A.S. et al. (2003) Redox-dependent downregulation of Rho by Rac. Nat. Cell Biol., 5, 236-241.
41. Lin, A. et al. (2002) The true face of JNK activation in apoptosis. Aging Cell, 1, 112-116.
42. Morel, Y. et al. (1999) An autoregulatory loop controlling CYP1A1 gene expression: role of H(2)O(2) and NFI. Mol. Cell. Biol., 19, 6825-6832.
43. Cao, C. et al. (2003) Catalase is regulated by ubiquitination and proteosomal degradation. Role of the c-Abl and Arg tyrosine kinases. Biochemistry, 42, 10348-10353.
44. Hu, Y. et al. (2012) K-ras(G12V) transformation leads to mitochondrial dysfunction and a metabolic switch from oxidative phosphorylation to glycolysis. Cell Res., 22, 399-412.
45. Kim, Y.S. et al. (2007) TNF-induced activation of the Nox1 NADPH oxidase and its role in the induction of necrotic cell death. Mol. Cell, 26, 675-687.
46. Shen, H.M. et al. (2004) Essential roles of receptor-interacting protein and TRAF2 in oxidative stress-induced cell death. Mol. Cell. Biol., 24, 5914-5922.
47. Gardner, A.M. et al. (1997) Apoptotic vs. nonapoptotic cytotoxicity induced by hydrogen peroxide. Free Radic. Biol. Med., 22, 73-83.
48. Bai, L. et al. (2012) A superoxide-mediated mitogen-activated protein kinase phosphatase-1 degradation and c-Jun NH(2)-terminal kinase activation pathway for luteolin-induced lung cancer cytotoxicity. Mol. Pharmacol., 81, 549-555.
49. Trachootham, D. et al. (2009) Targeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach? Nat. Rev. Drug Discov., 8, 579-591.