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英夫利昔单抗对紫外线B诱导的人乳头瘤病毒38 E6/E7感染角质形成细胞凋亡的影响

Effect of Infliximab on the UVB-Induced Apoptosis of Keratinocytes Infected by HPV38 E6/E7.

作者信息

Aubin François, Gheit Tarik, Prétet Jean Luc, Tommasino Massimo, Mougin Christiane

机构信息

Molecular and Cell Biology Laboratory, Université de Franche Comté, EA3181, SFR FED4234, Besançon, France ; Department of Dermatology, Centre Hospitalier Universitaire, 25030 Besançon, France.

出版信息

ISRN Dermatol. 2013;2013:907189. doi: 10.1155/2013/907189. Epub 2013 Feb 25.

DOI:10.1155/2013/907189
PMID:23533798
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3596906/
Abstract

The question of the effect of anti-TNF-alpha in skin carcinogenesis is especially relevant in view of the increased use of these drugs for the treatment of autoinflammatory immune diseases. Since ultraviolet radiation and human papillomavirus are involved in skin carcinogenesis, we wished to investigate the effect of TNF-alpha antagonists on the UVB-induced apoptosis of keratinocytes infected by HPV38. Our results indicate that anti-TNF agent, infliximab, does not contribute to the survival of HPV38-transduced keratinocytes with UVB-induced DNA damages.

摘要

鉴于抗TNF-α药物在自身炎症性免疫疾病治疗中的使用增加,抗TNF-α在皮肤癌发生中的作用问题尤为重要。由于紫外线辐射和人乳头瘤病毒参与皮肤癌发生,我们希望研究TNF-α拮抗剂对受HPV38感染的角质形成细胞UVB诱导凋亡的影响。我们的结果表明,抗TNF药物英夫利昔单抗不会促进受HPV38转导且有UVB诱导DNA损伤的角质形成细胞的存活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e676/3596906/870493050907/ISRN.DERMATOLOGY2013-907189.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e676/3596906/d0d2eebbcedb/ISRN.DERMATOLOGY2013-907189.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e676/3596906/870493050907/ISRN.DERMATOLOGY2013-907189.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e676/3596906/d0d2eebbcedb/ISRN.DERMATOLOGY2013-907189.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e676/3596906/870493050907/ISRN.DERMATOLOGY2013-907189.002.jpg

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Effect of Infliximab on the UVB-Induced Apoptosis of Keratinocytes Infected by HPV38 E6/E7.英夫利昔单抗对紫外线B诱导的人乳头瘤病毒38 E6/E7感染角质形成细胞凋亡的影响
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Loss of p53 or p73 in human papillomavirus type 38 E6 and E7 transgenic mice partially restores the UV-activated cell cycle checkpoints.在人乳头瘤病毒38型E6和E7转基因小鼠中,p53或p73缺失可部分恢复紫外线激活的细胞周期检查点。
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本文引用的文献

1
Case-control study of cutaneous human papillomaviruses in squamous cell carcinoma of the skin.皮肤鳞状细胞癌中人乳头瘤病毒的病例对照研究。
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NF-kappaB protects human papillomavirus type 38 E6/E7-immortalized human keratinocytes against tumor necrosis factor alpha and UV-mediated apoptosis.NF-κB 保护人乳头瘤病毒 38 型 E6/E7 永生化人角质形成细胞免受肿瘤坏死因子 α 和 UV 诱导的细胞凋亡。
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肿瘤坏死因子-α(TNF)抑制剂的癌症风险:阿达木单抗、依那西普和英夫利昔单抗的随机对照试验的荟萃分析,使用患者水平数据。
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E6 and E7 proteins from different beta-papillomaviruses types do not interfere in UVB-induced apoptosis of HaCaT keratinocytes.不同β型乳头瘤病毒的 E6 和 E7 蛋白不会干扰 HaCaT 角质形成细胞中 UVB 诱导的细胞凋亡。
Exp Dermatol. 2011 Jan;20(1):71-3. doi: 10.1111/j.1600-0625.2010.01197.x.
5
Impact of etanercept treatment on ultraviolet B-induced inflammation, cell cycle regulation and DNA damage.依那西普治疗对紫外线 B 诱导的炎症、细胞周期调控和 DNA 损伤的影响。
Br J Dermatol. 2011 Jan;164(1):110-5. doi: 10.1111/j.1365-2133.2010.10099.x.
6
Expression of human papillomavirus type 16 E7 oncoprotein alters keratinocytes expression profile in response to tumor necrosis factor-alpha.人乳头瘤病毒 16 型 E7 癌蛋白的表达改变角质形成细胞对肿瘤坏死因子-α的反应谱。
Carcinogenesis. 2010 Mar;31(3):521-31. doi: 10.1093/carcin/bgp333. Epub 2009 Dec 30.
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The impact of treatment with tumour necrosis factor-alpha antagonists on the course of chronic viral infections: a review of the literature.肿瘤坏死因子-α拮抗剂治疗对慢性病毒感染病程的影响:文献综述
Br J Dermatol. 2008 Dec;159(6):1217-28. doi: 10.1111/j.1365-2133.2008.08851.x. Epub 2008 Sep 25.
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Infliximab inhibits DNA repair in ultraviolet B-irradiated premalignant keratinocytes.英夫利昔单抗抑制紫外线B照射的癌前角质形成细胞中的DNA修复。
Exp Dermatol. 2008 Nov;17(11):933-8. doi: 10.1111/j.1600-0625.2008.00727.x. Epub 2008 Jun 14.
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TNF-alpha impairs the S-G2/M cell cycle checkpoint and cyclobutane pyrimidine dimer repair in premalignant skin cells: role of the PI3K-Akt pathway.肿瘤坏死因子-α损害癌前皮肤细胞中的S-G2/M细胞周期检查点和环丁烷嘧啶二聚体修复:PI3K-Akt信号通路的作用
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