Ionizing radiation suppresses FAP‐1 mRNA level in A549 cells via p53 activation

Yamada, Tōru; Maruyama, Muneharu; Fujita, Tadashi; Miyabayashi, Koutarou; Shinoda, Chie; Kawagishi, Yukio; Fujishita, Takashi; Hayashi, Ryuji; Miwa, Takeshi; Arai, Naoya; Matsui, Shoko; Sugiyama, Eiji; Kobayashi, Masashi

doi:10.1016/j.febslet.2006.07.003

Cited by 6 publications

(8 citation statements)

References 21 publications

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“…Consistent with these studies, we showed that knockdown of FAP-1 encouraged the cell surface display of Fas. Furthermore, the promoter of FAP-1 has been identified as a potential binding site for p53, and p53 activation suppresses the expression of FAP-1 (48,49). We found similar results in that the overexpression of p53 reduced the protein level of FAP-1.…”

Section: Discussionsupporting

confidence: 77%

Pigment Epithelial-derived Factor (PEDF)-triggered Lung Cancer Cell Apoptosis Relies on p53 Protein-driven Fas Ligand (Fas-L) Up-regulation and Fas Protein Cell Surface Translocation

Yao

Fang

et al. 2014

Journal of Biological Chemistry

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Background: PEDF has attracted attention for its direct antitumor effect. Results: The p53-mediated cell surface translocation of Fas and up-regulation of Fas-L contributes to PEDF-induced apoptosis. Conclusion: PEDF induces apoptosis by restoring the function of Fas death signaling in Fas-resistant lung cancer cells. Significance: Our findings provide a potential therapeutic strategy for Fas-resistant tumors resulting from a low level of cell surface Fas.

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Section: Discussionsupporting

confidence: 77%

Pigment Epithelial-derived Factor (PEDF)-triggered Lung Cancer Cell Apoptosis Relies on p53 Protein-driven Fas Ligand (Fas-L) Up-regulation and Fas Protein Cell Surface Translocation

Yao

Fang

et al. 2014

Journal of Biological Chemistry

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“…Fas mRNA and protein levels increased two-to fourfold after a respiratory syncytial virus infection (32). Fas was upregulated in response both to cigarette smoke extracts and to ionizing radiation (21,47). Inhibitors of epidermal growth factor receptor tyrosine kinase, such as gefitinib and ZD1839, and extracts of the Chinese herbs gossypol and casuarinin all upregulated Fas signaling and apoptosis (7,8,25,36).…”

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confidence: 99%

Streptococcal Pyrogenic Exotoxin B-Induced Apoptosis in A549 Cells Is Mediated through α _v β ₃ Integrin and Fas

et al. 2008

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Our previous work suggested that streptococcal pyrogenic exotoxin (SPE) B-induced apoptosis is mediated through a receptor-like mechanism. In this study, we have identified ␣ v ␤ 3 and Fas as the SPE B receptors for this function. The SPE B fragment without the RGD motif and G308S, a SPE B mutant with the RSD motif, induced less apoptosis than did native SPE B, suggesting that the RGD motif is critical for SPE B-induced apoptosis. Fluorescein isothiocyanate-SPE B binding assays and immunoprecipitation analysis showed that SPE B specifically interacted with ␣ v ␤ 3 . Anti-␣ v ␤ 3 antibody partially inhibited SPE B-induced apoptosis but had no effect on G308S-induced apoptosis. In addition, Fas binding to SPE B was verified in an affinity column and an immunoprecipitation analysis. Anti-Fas antibody inhibited SPE B-and G308S-induced apoptosis in a dose-dependent manner, suggesting that Fas-mediated SPE B-induced apoptosis also occurs RGD independently. Both anti-␣ v ␤ 3 and anti-Fas antibodies synergistically inhibited SPE B-induced apoptosis. The apoptotic cascades were activated by SPE B and G308S, with a little delay by the latter. After SPE B binding, the cell surface level of ␣ v ␤ 3 , but not of Fas, was decreased. The decreased ␣ v ␤ 3 level was restored by treatment with the proteasome inhibitor MG132, suggesting a SPE B-mediated endocytosis of integrin ␣ v ␤ 3 via the ubiquitin-proteasome system. Taken together, our results demonstrate that SPE B-induced apoptosis is mediated through ␣ v ␤ 3 integrin and Fas in a synergistic manner.Streptococcal pyrogenic exotoxin (SPE) B is an important virulence factor produced by group A streptococcus (GAS), a human pathogenic bacterium that causes infections of various severities (30). SPE B is a cysteine protease secreted as a 40-kDa zymogen that is autocatalytically converted to a 28-kDa mature form. Studies of cellular reactions of SPE B have focused on its protease activity (10,15,43). Its role as a ligand protein has not been critically evaluated. Our recent study showed that SPE B-induced apoptosis in human lung epithelial A549 cells is mediated through a receptor-like mechanism and a mitochondrion-dependent pathway and that the protease activity of SPE B is required to initiate apoptotic signaling, most likely by exposing the binding site for SPE B (44). However, the SPE B receptors and the molecular mechanism of SPE B interaction with its receptors remain to be explored.Three main SPE B variants have been identified in 200 GAS isolates of the speB gene (39). One variant contains an arginineglycine-aspartic acid (RGD) sequence and interacts with human integrins ␣ v ␤ 3 and ␣ IIb ␤ 3 . The GAS isolates that contain the RGD motif in SPE B are the most common cause of invasive diseases. Moreover, Kagawa et al. (23) demonstrated that the surface location of an RGD motif is a feature unique to SPE B among cysteine proteases and is linked to the pathogenesis of the most invasive strains of GAS. Therefore, understanding the role of the RGD motif in the interaction of...

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“…P53 mutations were associated with the development of multiple cancer types [22, 23]. The G72C single nucleotide polymorphism is located in the apoptosis-inducing region of the protein, and substitution of the G with a C nucleotide leads to an amino acid exchange from arginine to proline.…”

Section: Introductionmentioning

confidence: 99%

P27 and P53 Gene Polymorphisms and Restenosis following Coronary Implantation of Drug-Eluting Stents

et al. 2008

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Objective: Drug-eluting stents (DES) have reduced restenosis rates compared with bare-metal stents. P27 and P53 play important roles in the signal transduction leading to neointimal growth inhibition and induction of apoptosis of smooth muscle cells due to rapamycin and paclitaxel. We hypothesized that genetic variants of P27 and P53 influence the development of restenosis and the clinical outcome of patients receiving DES. Methods: Polymorphisms in the genes encoding for P27 and P53 were tested for their association with restenosis and major adverse cardiac events. P27 C-79T and P53 G72C polymorphism genotypes were determined in a series of 433 consecutive patients receiving DES. Follow-up angiography after 6 months was performed in 87% of the patients. Genotyping was performed with PCR-based methods. Results: For patients with the respective P27 C-79T and P53 G72C genotypes, the angiographic restenosis rates were between 5.0 and 22.0%, and the clinical restenosis rates were between 0.0 and 16.3%, without significant differences for the studied genotypes (p > 0.19). There was no association of the studied genotypes with the 1-year incidences of death and myocardial infarction. Conclusion: This study could not demonstrate a clinically relevant role of P27 and P53 polymorphisms in the processes leading to in-stent restenosis.

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Ionizing radiation suppresses FAP‐1 mRNA level in A549 cells via p53 activation

Cited by 6 publications

References 21 publications

Pigment Epithelial-derived Factor (PEDF)-triggered Lung Cancer Cell Apoptosis Relies on p53 Protein-driven Fas Ligand (Fas-L) Up-regulation and Fas Protein Cell Surface Translocation

Pigment Epithelial-derived Factor (PEDF)-triggered Lung Cancer Cell Apoptosis Relies on p53 Protein-driven Fas Ligand (Fas-L) Up-regulation and Fas Protein Cell Surface Translocation

Streptococcal Pyrogenic Exotoxin B-Induced Apoptosis in A549 Cells Is Mediated through α _v β ₃ Integrin and Fas

P27 and P53 Gene Polymorphisms and Restenosis following Coronary Implantation of Drug-Eluting Stents

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Ionizing radiation suppresses FAP‐1 mRNA level in A549 cells via p53 activation

Cited by 6 publications

References 21 publications

Pigment Epithelial-derived Factor (PEDF)-triggered Lung Cancer Cell Apoptosis Relies on p53 Protein-driven Fas Ligand (Fas-L) Up-regulation and Fas Protein Cell Surface Translocation

Pigment Epithelial-derived Factor (PEDF)-triggered Lung Cancer Cell Apoptosis Relies on p53 Protein-driven Fas Ligand (Fas-L) Up-regulation and Fas Protein Cell Surface Translocation

Streptococcal Pyrogenic Exotoxin B-Induced Apoptosis in A549 Cells Is Mediated through α v β 3 Integrin and Fas

P27 and P53 Gene Polymorphisms and Restenosis following Coronary Implantation of Drug-Eluting Stents

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Streptococcal Pyrogenic Exotoxin B-Induced Apoptosis in A549 Cells Is Mediated through α _v β ₃ Integrin and Fas