Extracellular generation of hydrogen peroxide is responsible for activation of EGF receptor by ultraviolet A radiation

Montfort, Claudia von; Fernau, Niklas S.; Beier, Juliane I.; Sies, Helmut; Klotz, Lars‐Oliver

doi:10.1016/j.freeradbiomed.2006.08.005

Cited by 24 publications

(9 citation statements)

References 38 publications

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“…8). A similar finding was reported for the epidermal growth 462 factor receptor whose activation by hydrogen peroxide in fibro-463 blasts required high millimolar H 2 O 2 concentrations unless a sen-464 sitizing PTPase inhibitor, orthovanadate, was co-applied [17]. We …”

supporting

confidence: 77%

Insulin-like modulation of Akt/FoxO signaling by copper ions is independent of insulin receptor

Hamann

Petroll

Grimm

et al. 2014

Archives of Biochemistry and Biophysics

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supporting

confidence: 77%

Insulin-like modulation of Akt/FoxO signaling by copper ions is independent of insulin receptor

Hamann

Petroll

Grimm

et al. 2014

Archives of Biochemistry and Biophysics

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“…Indeed, UVA activates EGFR (4,8,25) and h-catenin is a target of EGFR (9). Our study shows that, on UVA activation, EGFR targets the Y654 residue of h-catenin but not Y142 or Y86.…”

Section: Discussionmentioning

confidence: 66%

Epidermal Growth Factor Receptor/β-Catenin/T-Cell Factor 4/Matrix Metalloproteinase 1: A New Pathway for Regulating Keratinocyte Invasiveness after UVA Irradiation

et al. 2009

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Previous studies have established that UV irradiation results in epidermal growth factor receptor (EGFR) activation in keratinocytes. However, the signaling pathways and cellular effects related to this process remain incompletely elucidated. Herein, we describe for the first time that UVA-mediated EGFR activation results in B-catenin tyrosine phosphorylation at the Y654 residue responsible for the dissociation of E-cadherin/ A-catenin/B-catenin complexes. Moreover, UVA induces an EGFR-dependent, but Wnt-independent, B-catenin relocalization from the membrane to the nucleus followed by its association with T-cell factor 4 (TCF4). This newly formed B-catenin/TCF4 complex binds to a specific site on matrix metalloproteinase 1 (MMP1) promoter and governs MMP1 gene and protein expression, as well as cell migration in collagen and gelatin. Altogether, these results suggest that UVA stimulates keratinocyte invasiveness through two coordinated EGFR-dependent processes: loss of cell-to-cell contact due to B-catenin/E-cadherin/A-catenin dissociation and increased cell migration through extracellular matrix component degradation due to B-catenin/TCF4-dependent MMP1 regulation. These events may represent an important step in epidermis repair following UVA injury and their abnormal regulation could contribute to photoaging and photocarcinogenesis. [Cancer Res 2009;69(8):3291-9]

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“…The antioxidant property of C3G is confirmed in this study and we show that C3G effectively blocks ethanol-induced ROS production in breast cancer cells. ROS is reported to be involved in the activation of EGFR [44]. To evaluate the involvement of ROS, we compared the effect of C3G with other antioxidants.…”

Section: Discussionmentioning

confidence: 99%

Cyanidin-3-Glucoside inhibits ethanol-induced invasion of breast cancer cells overexpressing ErbB2

et al. 2010

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BackgroundEthanol is a tumor promoter. Both epidemiological and experimental studies suggest that ethanol may enhance the metastasis of breast cancer cells. We have previously demonstrated that ethanol increased the migration/invasion of breast cancer cells expressing high levels of ErbB2. Amplification of ErbB2 is found in 20-30% of breast cancer patients and is associated with poor prognosis. We sought to identify agents that can prevent or ameliorate ethanol-induced invasion of breast cancer cells. Cyanidin-3-glucoside (C3G), an anthocyanin present in many vegetables and fruits, is a potent natural antioxidant. Ethanol exposure causes the accumulation of intracellular reactive oxygen species (ROS). This study evaluated the effect of C3G on ethanol-induced breast cancer cell migration/invasion.ResultsC3G attenuated ethanol-induced migration/invasion of breast cancer cells expressing high levels of ErbB2 (BT474, MDA-MB231 and MCF7ErbB2) in a concentration dependent manner. C3G decreased ethanol-mediated cell adhesion to the extracellular matrix (ECM) as well as the amount of focal adhesions and the formation of lamellipodial protrusion. It inhibited ethanol-stimulated phosphorylation of ErbB2, cSrc, FAK and p130Cas, as well as interactions among these proteins. C3G abolished ethanol-mediated p130Cas/JNK interaction.ConclusionsC3G blocks ethanol-induced activation of the ErbB2/cSrc/FAK pathway which is necessary for cell migration/invasion. C3G may be beneficial in preventing/reducing ethanol-induced breast cancer metastasis.

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Extracellular generation of hydrogen peroxide is responsible for activation of EGF receptor by ultraviolet A radiation

Cited by 24 publications

References 38 publications

Insulin-like modulation of Akt/FoxO signaling by copper ions is independent of insulin receptor

Insulin-like modulation of Akt/FoxO signaling by copper ions is independent of insulin receptor

Epidermal Growth Factor Receptor/β-Catenin/T-Cell Factor 4/Matrix Metalloproteinase 1: A New Pathway for Regulating Keratinocyte Invasiveness after UVA Irradiation

Cyanidin-3-Glucoside inhibits ethanol-induced invasion of breast cancer cells overexpressing ErbB2

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