title: JWA as a novel molecule involved in oxidative stress-associated signal pathway in myelogenous leukemia cells.
abstract: Previous data showed that JWA might be a novel environmental responsive gene regulated by environmental stressors such as heat shock and oxidative stress. However, the molecular mechanism underlying JWA gene function involved in oxidative stress is still unknown. In this study, the potential role of JWA was further investigated in hydrogen peroxide (H2O2) induced DNA damage and cell apoptosis in K562 cells. Series of the oxidative stress models were established to observe if JWA was involved in DNA damage or cell apoptosis induced by H2O2 exposure. These results indicated that the inhibitory effect on K562 cells' viability induced by H2O2 was concentration and time dependent. JWA was more sensitive to H2O2 (0.01 mmol/L) than the heat-shock proteins (hsp70 and hsp27), and its expression pattern was similar to that of hsp70. In addition, JWA, hsp70, hsp27, and p53 were overexpressed and the expression patterns of JWA, hsp70, and p53 were similar during cell apoptosis. H2O2 led to the cleavage and activation of procaspase-3. In conclusion, these results suggested that JWA might be an effective environmental responsive gene that functions as a parallel with hsp70 in oxidative stress-responsive pathways in K562 cells. Like hsp70, JWA might enhance intracellular defenses and function against H2O2-induced oxidative stress in leukemia cells. At the same time, JWA was involved in the p53-associated signal pathways of oxidative stress-induced apoptosis, which is also caspase-3 dependent.
authors.affiliation: Department of Molecular Cell Biology and Toxicology, Jiangsu Provincial Key Laboratories of Human Functional Genomics and of Applied Toxicology, School of Public Health, Nanjing Medical University, Nanjing, People's Republic of China.
authors.forename: Ting
authors.initials: T
authors.lastname: Zhu
authors.forename: Rui
authors.initials: R
authors.lastname: Chen
authors.forename: Aiping
authors.initials: A
authors.lastname: Li
authors.forename: Jia
authors.initials: J
authors.lastname: Liu
authors.forename: Dengan
authors.initials: D
authors.lastname: Gu
authors.forename: Qizhan
authors.initials: Q
authors.lastname: Liu
authors.forename: Hebron
authors.initials: H
authors.lastname: C Chang
authors.forename: Jianwei
authors.initials: J
authors.lastname: Zhou
mesh_terms: D017209:Apoptosis / Q000502:physiology; D053148:Caspase 3; D020169:Caspases / Q000096:biosynthesis; D002470:Cell Survival / Q000502:physiology; D004249:DNA Damage / Q000502:physiology; D005786:Gene Expression Regulation; D016158:Genes, p53 / Q000502:physiology; D018840:HSP70 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D006801:Humans; D006861:Hydrogen Peroxide; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000502:physiology*; D020014:K562 Cells; D026901:Membrane Transport Proteins; D016877:Oxidants; D018384:Oxidative Stress / Q000502:physiology*; D015398:Signal Transduction
chemical_list: C484566:ARL6IP5 protein, human; D018840:HSP70 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D047908:Intracellular Signaling Peptides and Proteins; D026901:Membrane Transport Proteins; D016877:Oxidants; D006861:Hydrogen Peroxide; C505407:CASP3 protein, human; D053148:Caspase 3; D020169:Caspases