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2.
Cancer Gene Ther ; 27(7-8): 619-623, 2020 08.
Artigo em Inglês | MEDLINE | ID: mdl-31664166

RESUMO

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been reported to kill a wide variety of tumor cells with minimal effects on normal cell. However, renal cell carcinoma (RCC) cells 786-0 and OS-RC-2 were resistant to TRAIL. The present study examines the potential of combining polyphenolic compound resveratrol (RES) with TRAIL. We found that RES can sensitize RCC cells to TRAIL-induced death. Electron microscopy analyses showed that RES plus TRAIL can induce both autophagy and apoptosis in RCC cells. It was proved that the apoptosis is caspase-dependent and the activation of caspase-8, caspase-9, and caspase-3 was involved in this process. Besides, we also found that XIAP expression was significantly inhibited after RES plus TRAIL treatment in RCC cells. Furthermore, a fiber-modified replication-deficient adenovirus Ad5/35-TRAIL was generated to test the synergistic effect of RES and TRAIL in vivo. Our data demonstrated that RES plus Ad5/35-TRAIL significantly inhibited RCC xenograft growth in nude mice. These results suggest the possibility of a new combination therapeutic leading to the improvement of RCC treatment.


Assuntos
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Carcinoma de Células Renais/tratamento farmacológico , Neoplasias Renais/tratamento farmacológico , Resveratrol/uso terapêutico , Ligante Indutor de Apoptose Relacionado a TNF/uso terapêutico , Animais , Apoptose , Proteínas Reguladoras de Apoptose , Autofagia , Carcinoma de Células Renais/fisiopatologia , Linhagem Celular Tumoral , Humanos , Neoplasias Renais/fisiopatologia , Camundongos , Camundongos Nus , Ensaios Antitumorais Modelo de Xenoenxerto
4.
Biochem Biophys Res Commun ; 511(4): 935-940, 2019 04 16.
Artigo em Inglês | MEDLINE | ID: mdl-30853180

RESUMO

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal).. This article has been retracted at the request of < the Editor in Chief. The Editor in Chief has been made aware of numerous problems with this paper regarding authorship, poor or insufficient supervision of researchers and the unauthorized use of data acquired from a lab visit by one of the authors.


Assuntos
Regulação da Expressão Gênica no Desenvolvimento , Proteína com Dedos de Zinco da Leucemia Promielocítica/genética , Linfócitos T/citologia , Animais , Contagem de Células , Autorrenovação Celular , Deleção de Genes , Camundongos , Camundongos Endogâmicos C57BL , Linfócitos T/metabolismo , Timócitos/citologia , Timócitos/metabolismo , Timo/citologia , Timo/crescimento & desenvolvimento , Timo/metabolismo
6.
Front Microbiol ; 9: 1865, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30174659

RESUMO

Hepatitis A virus (HAV) belongs to the family Picornaviridae. It is the pathogen of acute viral hepatitis caused by fecal-oral transmission. RNA viruses are sensed by pathogen-associated pattern recognition receptors (PRRs) such as Toll-like receptor 3 (TLR3), retinoic acid-inducible gene I (RIG-I), and melanoma differentiation-associated gene 5 (MDA5). PRR activation leads to production of type 1 interferon (IFN-α/ß), serving as the first line of defense against viruses. However, HAV has developed various strategies to compromise the innate immune system and promote viral propagation within the host cells. The long coevolution of HAV in hosts has prompted the development of effective immune antagonism strategies that actively fight against host antiviral responses. Proteases encoded by HAV can cleave the mitochondrial antiviral signaling protein (MAVS, also known as IPS-1, VISA, or Cardif), TIR domain- containing adaptor inducing IFN-ß (TRIF, also known as TICAM-1) and nuclear factor-κB (NF-κB) essential modulator (NEMO), which are key adaptor proteins in RIG-I-like receptor (RLR), TLR3 and NF-κB signaling, respectively. In this mini-review, we summarize all the recent progress on the interaction between HAV and the host, especially focusing on how HAV abrogates the antiviral effects of the innate immune system.

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