Antioxidant Role of p53 and of Its Target TP53INP1

Seillier, Marion; Peuget, Sylvain; Dusetti, Nelson J; Carrier, Alice

doi:10.5772/50790

Cited by 5 publications

(4 citation statements)

References 64 publications

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“…The TP53 gene, known as "the guardian of genome", has been shown to be induced in response to DNA damage and its induction results from different processes including oxidative modifications. 73 However, here we did not observe a significant increase in the expression of TP53 following treatment with E. tirucalli, which may be related to the short-term exposure used here.…”

Section: Discussioncontrasting

confidence: 72%

Euphorbia tirucalli aqueous extract induces cytotoxicity, genotoxicity and changes in antioxidant gene expression in human leukocytes

et al. 2015

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Section: Discussioncontrasting

confidence: 72%

Euphorbia tirucalli aqueous extract induces cytotoxicity, genotoxicity and changes in antioxidant gene expression in human leukocytes

et al. 2015

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“…A connection might be the tumor protein 53 inducible protein 1 (TP53INP1). TP53INP1 is strongly induced by Fv1 on the gene expression level and it is able to play an autonomous role in cell cycle regulation and mediates several of its functions independently of p53 [ 31 ]. Another player might be CDC20.…”

Section: Discussionmentioning

confidence: 99%

Molecular Mechanisms by Which a Fucus vesiculosus Extract Mediates Cell Cycle Inhibition and Cell Death in Pancreatic Cancer Cells

Geisen

Zenthoefer²,

Peipp

et al. 2015

Marine Drugs

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Pancreatic cancer is one of the most aggressive cancer entities, with an extremely poor 5-year survival rate. Therefore, novel therapeutic agents with specific modes of action are urgently needed. Marine organisms represent a promising source to identify new pharmacologically active substances. Secondary metabolites derived from marine algae are of particular interest. The present work describes cellular and molecular mechanisms induced by an HPLC-fractionated, hydrophilic extract derived from the Baltic brown seaweed Fucus vesiculosus (Fv1). Treatment with Fv1 resulted in a strong inhibition of viability in various pancreatic cancer cell lines. This extract inhibited the cell cycle of proliferating cells due to the up-regulation of cell cycle inhibitors, shown on the mRNA (microarray data) and protein level. As a result, cells were dying in a caspase-independent manner. Experiments with non-dividing cells showed that proliferation is a prerequisite for the effectiveness of Fv1. Importantly, Fv1 showed low cytotoxic activity against non-malignant resting T cells and terminally differentiated cells like erythrocytes. Interestingly, accelerated killing effects were observed in combination with inhibitors of autophagy. Our in vitro data suggest that Fv1 may represent a promising new agent that deserves further development towards clinical application.

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“…We might hypothesize that TP53inp1 -mediated autophagy could be part of the cellular response against oxidative stress that protects against cell organelle failure by inducing death of cells with excessive radiation damage. Impaired autophagy can induce ROS accumulation and DNA damage [ 32 ]. TP53inp1 could be a partner in displacing p62 from LC3, therefore enhancing degradation of proteins, for example, antiapoptotic proteins, whose depletion would lead to cell death [ 4 ].…”

Section: Discussionmentioning

confidence: 99%

TP53inp1 Gene Is Implicated in Early Radiation Response in Human Fibroblast Cells

Sándor

Schilling-Tóth

Kis

et al. 2015

IJMS

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Tumor protein 53-induced nuclear protein-1 (TP53inp1) is expressed by activation via p53 and p73. The purpose of our study was to investigate the role of TP53inp1 in response of fibroblasts to ionizing radiation. γ-Ray radiation dose-dependently induces the expression of TP53inp1 in human immortalized fibroblast (F11hT) cells. Stable silencing of TP53inp1 was done via lentiviral transfection of shRNA in F11hT cells. After irradiation the clonogenic survival of TP53inp1 knockdown (F11hT-shTP) cells was compared to cells transfected with non-targeting (NT) shRNA. Radiation-induced senescence was measured by SA-β-Gal staining and autophagy was detected by Acridine Orange dye and microtubule-associated protein-1 light chain 3 (LC3B) immunostaining. The expression of TP53inp1, GDF-15, and CDKN1A and alterations in radiation induced mitochondrial DNA deletions were evaluated by qPCR. TP53inp1 was required for radiation (IR) induced maximal elevation of CDKN1A and GDF-15 expressions. Mitochondrial DNA deletions were increased and autophagy was deregulated following irradiation in the absence of TP53inp1. Finally, we showed that silencing of TP53inp1 enhances the radiation sensitivity of fibroblast cells. These data suggest functional roles for TP53inp1 in radiation-induced autophagy and survival. Taken together, we suppose that silencing of TP53inp1 leads radiation induced autophagy impairment and induces accumulation of damaged mitochondria in primary human fibroblasts.

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Antioxidant Role of p53 and of Its Target TP53INP1

Cited by 5 publications

References 64 publications

Euphorbia tirucalli aqueous extract induces cytotoxicity, genotoxicity and changes in antioxidant gene expression in human leukocytes

Euphorbia tirucalli aqueous extract induces cytotoxicity, genotoxicity and changes in antioxidant gene expression in human leukocytes

Molecular Mechanisms by Which a Fucus vesiculosus Extract Mediates Cell Cycle Inhibition and Cell Death in Pancreatic Cancer Cells

TP53inp1 Gene Is Implicated in Early Radiation Response in Human Fibroblast Cells

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