NADPH oxidase and ERK1/2 are involved in cadmium induced-STAT3 activation in HepG2 cells

Souza, Verónica; Escobar, Ma. del Carmen; Bucio, Leticia; Hernández, Elizabeth; Gómez-Quiroz, Luís Enrique; Ruiz, Ma Concepción Gutiérrez

doi:10.1016/j.toxlet.2009.02.021

Cited by 54 publications

(29 citation statements)

References 48 publications

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“…NADPH-dependent ROS production is also described in Cd-exposed hepatocytes (Fotakis et al 2005). This ROS production could trigger signaling leading to protective measures, as reported by Souza et al (2009) in HepG2 cells. Alternatively, production of excess ROS may lead to Cd-induced toxicity, as shown by Rockwell et al (2004) in mouse neuronal cells.…”

Section: Induction Of Nadph Oxidasesmentioning

confidence: 74%

“…signaling play an important role (Thévenod 2009 and references herein). The activation of the p38-MAPK signal cascade during Cd stress leads to both pro-and anti-apoptotic events as it can trigger both caspase-3 and HSP70 (70 kD Heat Shock Proteins) in different organisms (Kefaloyianni et al 2005;Valbonesi et al 2008;Souza et al 2009). Cd increases JNK signaling via changes in [Ca 2? ]…”

Section: Cadmium: An Oxidative Challengementioning

confidence: 99%

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Cadmium stress: an oxidative challenge

et al. 2010

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At the cellular level, cadmium (Cd) induces both damaging and repair processes in which the cellular redox status plays a crucial role. Being not redox-active, Cd is unable to generate reactive oxygen species (ROS) directly, but Cd-induced oxidative stress is a common phenomenon observed in multiple studies. The current review gives an overview on Cd-induced ROS production and anti-oxidative defense in organisms under different Cd regimes. Moreover, the Cd-induced oxidative challenge is discussed with a focus on damage and signaling as downstream responses. Gathering these data, it was clear that oxidative stress related responses are affected during Cd stress, but the apparent discrepancies observed in between the different studies points towards the necessity to increase our knowledge on the spatial and temporal ROS signature under Cd stress. This information is essential in order to reveal the exact role of Cd-induced oxidative stress in the modulation of downstream responses under a diverse array of conditions.

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Section: Induction Of Nadph Oxidasesmentioning

confidence: 74%

Section: Cadmium: An Oxidative Challengementioning

confidence: 99%

Cadmium stress: an oxidative challenge

et al. 2010

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“…Angiotensin II, the most active factor in this system, is a well-known oxidative stress inducer which increases the generation of superoxide anion, hydrogen peroxide and hydroxyl radicals by activating the NADPH oxidase enzyme (Cai et al, 2003) which is the main source of cadmium-induced production of reactive oxygen species (Souza et al, 2009;Banakou and Dailianis, 2010). Also, angiotensin II activates inflammatory cascades with increased production of the proinflammatory cytokine, TNF-α which is responsible for further renal tissue injury (Cau et al, 2009;Hayashi et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Protective effect of telmisartan against cadmium-induced nephrotoxicity in mice

Fouad

Jresat

2011

Life Sciences

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“…Target proteins transcribed by activated STAT3 are implicated in fundamental events of tumor development, including its proliferation, survival, invasion and angiogenesis (Groner et al, 2008). Recent findings show that STAT3 can also be activated by reactive oxygen species (ROS) generated by NADPH oxidase (Lee et al, 2007;Souza et al, 2009;Yoon et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

NF-κB and STAT3 cooperatively induce IL6 in starved cancer cells

et al. 2011

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A number of genes involved in tumorigenesis have been known to be controlled by signal transducer and activator of transcription 3 (STAT3) and NF-jB, either synergistically or individually. In starved cancer cells, we found that NF-jB was activated through endoplasmic reticulum stress signals, which depend on reactive oxygen species, cytosolic calcium and preserved translation of NF-jB p65 subunit, but independent of IjBa serine phosphorylation, thereby resulting in IL6 induction. STAT3 was required for proper induction of IL6 by NF-jB. They existed as identical nuclear complexes in proximal IL6 promoters, and STAT3 had critical roles in binding to IL6 promoters as well as nuclear retention of NF-jB. The conditioned media from starved cancer cells contained various secretory factors, such as IL6, IL9, VWF (von Willebrand factor), FREM1 (FRAS1 related extracellular matrix 1), SAA1 (serum amyloid A1), SDK1 (sidekick homolog 1) and ADAM12 (ADAM metallopeptidase domain 12), induced by NF-jB and STAT3 and promoted clonogenic capacities of cancer cells, and proliferation and migration of human umbilical vein endothelial cells. These results suggest novel survival strategies of cancer cells by which two oncogenic transcriptional factors, NF-jB and STAT3, are activated simultaneously by an intrinsic mechanism during stressful conditions of cancer cells, and they cooperatively induce various survival factors.

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NADPH oxidase and ERK1/2 are involved in cadmium induced-STAT3 activation in HepG2 cells

Cited by 54 publications

References 48 publications

Cadmium stress: an oxidative challenge

Cadmium stress: an oxidative challenge

Protective effect of telmisartan against cadmium-induced nephrotoxicity in mice

NF-κB and STAT3 cooperatively induce IL6 in starved cancer cells

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