Salicylic acid increases the contents of glutathione and ascorbate and temporally regulates the related gene expression in salt-stressed wheat seedlings
GENE
Authors: Li, Gezi; Peng, Xiaoqi; Wei, Liting; Kang, Guozhang
Abstract
Exogenous salicylic acid (SA) significantly improved abiotic tolerance in higher plants, and ascorbate (ASA) and glutathione (GSH) play important roles in abiotic tolerance. In this study, SA (0.5 mM) markedly increased the contents of ASA and GSH in SA-treated plants during salt stress (250 mM NaCl). The transcript levels of the genes encoding ASA and GSH cycle enzymes were measured using quantitative real-time PCR. The results indicated that, during salt stress, exogenous SA significantly enhanced the transcripts of glutathione peroxidase (GPX1), phospholipid hydroperoxide glutathione peroxidase (GPX2) and dehydroascorbate reductase (DHAR) genes at 12 h, glutathione reductase (GR) at 24 h, 48 h and 72 h, glutathione-S-transferase 1 (GST1), 2 (GST2), monodehydroascorbate reductase (MDHAR) and glutathione synthetase (GS) at the 48 h and 72 h after salt stress, respectively. The results implied that SA temporally regulated the transcript levels of the genes encoding ASA-GSH cycle enzymes, resulting in the increased contents of GSH and ASA and enhanced salt tolerance. (C) 2013 Elsevier B.V. All rights reserved.
GPx2 Suppression of H2O2 Stress Links the Formation of Differentiated Tumor Mass to Metastatic Capacity in Colorectal Cancer
CANCER RESEARCH
Authors: Emmink, Benjamin L.; Laoukili, Jamila; Kipp, Anna P.; Koster, Jan; Govaert, Klaas M.; Fatrai, Szabolcs; Verheem, Andre; Steller, Ernst J. A.; Brigelius-Flohe, Regina; Jimenez, Connie R.; Rinkes, Inne H. M. Borel; Kranenburg, Onno
Abstract
Colorectal tumorigenesis is accompanied by the generation of oxidative stress, but how this controls tumor development is poorly understood. Here, we studied how the H2O2-reducing enzyme glutathione peroxidase 2 (GPx2) regulates H2O2 stress and differentiation in patient-derived "colonosphere" cultures. GPx2 silencing caused accumulation of radical oxygen species, sensitization to H2O2-induced apoptosis, and strongly reduced clone-and metastasis-forming capacity. Neutralization of radical oxygen species restored clonogenic capacity. Surprisingly, GPx2-suppressed cells also lacked differentiation potential and formed slow-growing undifferentiated tumors. GPx2 overexpression stimulated multilineage differentiation, proliferation, and tumor growth without reducing the tumor-initiating capacity. Finally, GPx2 expression was inversely correlated with H2O2-stress signatures in human colon tumor cohorts, but positively correlated with differentiation and proliferation. Moreover, high GPx2 expression was associated with early tumor recurrence, particularly in the recently identified aggressive subtype of human colon cancer. We conclude that H2O2 neutralization by GPx2 is essential for maintaining clonogenic and metastatic capacity, but also for the generation of differentiated proliferating tumor mass. The results reveal an unexpected redox-controlled link between tumor mass formation and metastatic capacity. (C) 2014 AACR.