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1.
Chem Commun (Camb) ; 56(16): 2495-2498, 2020 Feb 25.
Artigo em Inglês | MEDLINE | ID: mdl-32003367

RESUMO

Herein, we report the photocatalytic decarboxylative alkenylation reactions of N-(acyloxy)phthalimide derived from α-amino and α-hydroxy acids with 1,1-diarylethene, and with cinnamic acid derivatives through double decarboxylation, using sodium iodide and triphenylphosphine as redox catalysts. The reaction proceeds under mild irradiation conditions with visible blue light (440 nm or 456 nm) in an acetone solvent without recourse to transition-metal or organic dye based photoredox catalysts. The reaction proceeds via photoactivation of a transiently self-assembled chromophore from N-(acyloxy)phthalimide and NaI/PPh3. Solvation plays a crucial role in the reactivity.


Assuntos
Aminoácidos/química , Hidroxiácidos/química , Compostos Organofosforados/química , Iodeto de Sódio/química , Alquilação , Catálise , Descarboxilação , Estrutura Molecular , Oxirredução , Processos Fotoquímicos
2.
Chem Commun (Camb) ; 56(11): 1693-1696, 2020 Feb 06.
Artigo em Inglês | MEDLINE | ID: mdl-31939945

RESUMO

Asymmetric conjugate addition of PhMe2SiBPin to a wide range of N-heteroaryl alkenes proceeded in the presence of a copper catalyst coordinated with an easily accessible chiral phosphoramidite ligand to afford useful ß-silyl N-heteroarenes in high yields (up to 96%) and excellent enantioselectivities (up to 97% ee).

3.
Nat Microbiol ; 5(2): 272-281, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31959973

RESUMO

Innate and adaptive immune responses that prime myeloid cells, such as macrophages, protect against pathogens1,2. However, if left uncontrolled, these responses may lead to detrimental inflammation3. Macrophages, particularly those resident in tissues, must therefore remain quiescent between infections despite chronic stimulation by commensal microorganisms. The genes required for quiescence of tissue-resident macrophages are not well understood. Autophagy, an evolutionarily conserved cellular process by which cytoplasmic contents are targeted for lysosomal digestion, has homeostatic functions including maintenance of protein and organelle integrity and regulation of metabolism4. Recent research has shown that degradative autophagy, as well as various combinations of autophagy genes, regulate immunity and inflammation5-12. Here, we delineate a function of the autophagy proteins Beclin 1 and FIP200-but not of other essential autophagy components ATG5, ATG16L1 or ATG7-in mediating quiescence of tissue-resident macrophages by limiting the effects of systemic interferon-γ. The perturbation of quiescence in mice that lack Beclin 1 or FIP200 in myeloid cells results in spontaneous immune activation and resistance to Listeria monocytogenes infection. While antibiotic-treated wild-type mice display diminished macrophage responses to inflammatory stimuli, this is not observed in mice that lack Beclin 1 in myeloid cells, establishing the dominance of this gene over effects of the bacterial microbiota. Thus, select autophagy genes, but not all genes essential for degradative autophagy, have a key function in maintaining immune quiescence of tissue-resident macrophages, resulting in genetically programmed susceptibility to bacterial infection.

4.
Huan Jing Ke Xue ; 40(7): 2994-3000, 2019 Jul 08.
Artigo em Chinês | MEDLINE | ID: mdl-31854696

RESUMO

This study selected a rubber tire manufacturing factory located in the North China Plain, and conducted ambient volatile organic compounds (VOCs) observation tests, and calculated the emission of VOCs based on the inverse-dispersion calculation method. The monitoring results found significant differences in both VOC concentrations and chemical composition between the up-wind (background) and the downwind receptors. The average concentrations of VOCs measured by the background and receptors were 53.8 µg·m-3 and 127.5 µg·m-3, respectively. Propane (7.2 µg·m-3), cetone (7.5 µg·m-3), nonanal (12.7 µg·m-3), n-butane (4.9 µg·m-3), and acetaldehyde (2.7 µg·m-3) were the dominant components of background VOCs, and nonanal (43.5 µg·m-3), propane (11.4 µg·m-3), acetaldehyde (7.4 µg·m-3), hexane (11.9 µg·m-3), and n-butane (7.3 µg·m-3) were the dominant components of receptor VOCs. The difference in VOCs between the background and receptors is considered to reflect contributions from the factory, the main components of which were of alkanes (31.39%) and oxygenated organic compounds (33.15%). Using the ISC3 model, the relation coefficient γ between the downwind VOCs increment and the emissions of the factory was calculated for each receptor of each test based on the hourly average meteorological conditions during the observation period. Combining the relation coefficient γ with the difference in VOCs between the receptor and the background, we calculated VOC emission amounts from this factory of 152.8±188.2 t·a-1 and a VOC emission factor (EF) for the rubber tire manufacturing industry of VOC 101.9 g·tire-1. Our estimated EF was loser to EF of U. S. AP42 (55 g·tire-1), but greatly lower than the EF of China's reference (900 g·tire-1). Although our calculations had a relatively higher standard deviation, these results are helpful for better understanding the emission of VOCs from the rubber manufacturing industry. Based on our calculated EF, China's national VOCs emissions from the rubber tire manufacturing industry would be approximately 62.13 kt·a-1, which represents a significant potential contribution to ozone formation (130.87 kt·a-1), but the organic aerosol formation potential is small (0.86 kt·a-1).

5.
Huan Jing Ke Xue ; 40(10): 4594-4603, 2019 Oct 08.
Artigo em Chinês | MEDLINE | ID: mdl-31854828

RESUMO

To improve the pollution signature database for polycyclic aromatic hydrocarbons (PAHs) in typical industrial areas in China, surface soil samples were collected from four typical petroleum-processing industrial areas of Chengdu. The concentration and composition of 16 PAHs listed for prior control by the United States Environmental Protection Agency (US EPA) were determined using high-performance liquid chromatography (HPLC). The result showed that the concentration of PAHs in surface soils of the four industrial areas ranged from 191.2 to 1604.2 µg·kg-1, with an average of (583.6±365.6) µg·kg-1. The PAHs in the present study were mainly composed of medium-molecular-weight PAHs and high-molecular-weight PAHs. Among the PAHs detected in the study soils, phenanthrene (PHE), pyrene (PYR), fluoranthene (FLT), and benzo[b]fluoranthene (BbF) were the major pollutants presenting a potential pollution risk. Selected mathematical statistical methods were used to analyze the relationship between soil organic matter (SOM), soil particle diameter and PAH content, and to simultaneously identify the factors influencing PAHs in the soils. SOM was shown to be a favorable absorbent, predicting the migration and transformation behavior of PAHs in surface soil and soil ecological risk (i.e., PAH carcinogenicity) to some extent. Compared with SOM, the correlation between PAHs and soil particle size was relatively low, showing a weak positive correlation with silt, a weakly negatively correlation with clay, and no significant correlation with sand. These results provide a basis for soil remediation practices and further research in such industrial areas.

6.
Proc Natl Acad Sci U S A ; 116(33): 16497-16506, 2019 Aug 13.
Artigo em Inglês | MEDLINE | ID: mdl-31346084

RESUMO

Host inflammatory responses must be tightly regulated to ensure effective immunity while limiting tissue injury. IFN gamma (IFNγ) primes macrophages to mount robust inflammatory responses. However, IFNγ also induces cell death, and the pathways that regulate IFNγ-induced cell death are incompletely understood. Using genome-wide CRISPR/Cas9 screening, we identified autophagy genes as central mediators of myeloid cell survival during the IFNγ response. Hypersensitivity of autophagy gene-deficient cells to IFNγ was mediated by tumor necrosis factor (TNF) signaling via receptor interacting protein kinase 1 (RIPK1)- and caspase 8-mediated cell death. Mice with myeloid cell-specific autophagy gene deficiency exhibited marked hypersensitivity to fatal systemic TNF administration. This increased mortality in myeloid autophagy gene-deficient mice required the IFNγ receptor, and mortality was completely reversed by pharmacologic inhibition of RIPK1 kinase activity. These findings provide insight into the mechanism of IFNγ-induced cell death via TNF, demonstrate a critical function of autophagy genes in promoting cell viability in the presence of inflammatory cytokines, and implicate this cell survival function in protection against mortality during the systemic inflammatory response.

7.
Am J Otolaryngol ; 40(5): 615-625, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31128861

RESUMO

PURPOSE: Laryngeal squamous-cell carcinoma (LSCC) is the second most common malignant tumor of head and neck squamous cell carcinoma. The study was aimed to identify key long non-coding RNAs (lncRNAs) biomarkers for LSCC. METHODS: Differentially expressed lncRNAs (DElncRNAs) and mRNAs (DEmRNAs) between LSCC and adjacent tissues were obtained based on The Cancer Genome Atlas. DElncRNA-DEmRNAs co-expression and DElncRNA-nearby-target DEmRNA interaction networks were constructed. Receiver operating characteristic and survival analysis were performed. A published dataset were as used to validate the result of bioinformatics analysis. RESULTS: We obtained 1103 DEmRNAs and 306 DElncRNAs between LSCC and adjacent tissues. A total of 338 DElncRNA-DEmRNA co-expression pairs and 229 DElncRNA-nearby-target DEmRNA pairs were obtained. Ten DElncRNAs and six DEmRNAs has great diagnostic value for LSCC. HOXB9 has potential prognostic value for LSCC. The results of GSE84957 validation were generally consistent with our results. CONCLUSION: Our study provided clues for understanding the mechanism and developing potential biomarkers for LSCC.


Assuntos
Regulação Neoplásica da Expressão Gênica , Neoplasias Laríngeas/genética , RNA Longo não Codificante/genética , RNA Mensageiro/genética , Carcinoma de Células Escamosas de Cabeça e Pescoço/genética , Biomarcadores Tumorais/genética , Biologia Computacional , Bases de Dados Factuais , Perfilação da Expressão Gênica , Redes Reguladoras de Genes , Genoma Humano , Humanos , Neoplasias Laríngeas/mortalidade , Prognóstico , Reprodutibilidade dos Testes , Carcinoma de Células Escamosas de Cabeça e Pescoço/mortalidade , Carcinoma de Células Escamosas de Cabeça e Pescoço/patologia
8.
Autophagy ; 15(11): 1917-1934, 2019 11.
Artigo em Inglês | MEDLINE | ID: mdl-30898011

RESUMO

Macroautophagy/autophagy is a cellular process in which cytosolic contents are degraded by lysosome in response to various stress conditions. Apart from its role in the maintenance of cellular homeostasis, autophagy also involves in regulation of cell cycle progression under nutrient-deprivation conditions. However, whether and how autophagy is regulated by the cell cycle especially during mitosis remains largely undefined. Here we show that WIPI2/ATG18B (WD repeat domain, phosphoinositide interacting 2), an autophagy-related (ATG) protein that plays a critical role in autophagosome biogenesis, is a direct substrate of CUL4-RING ubiquitin ligases (CRL4s). Upon mitosis induction, CRL4s are activated via neddylation, and recruit WIPI2 via DDB1 (damage specific DNA binding protein 1), leading to polyubiquitination and proteasomal degradation of WIPI2 and suppression of autophagy. The WIPI2 protein level and autophagy during mitosis could be rescued by knockdown of CRL4s or treatment with MLN4924/Pevonedistat, a selective inhibitor of CRLs, via suppression of NAE1 (NEDD8 activating enzyme E1 subunit 1). Moreover, restoration of WIPI2 rescues autophagy during mitosis and leads to mitotic slippage and cell senescence. Our study thus discovers a novel function of CRL4s in autophagy by targeting WIPI2 for polyubiquitination and proteasomal degradation during mitosis. Abbreviations: ACTB, actin beta; ATG, autophagy-related; AMPK, AMP-activated protein kinase; AURKB/ARK2, aurora kinase B; BafA1, bafilomycin A1; CCNB1, cyclin B1; CDK1, cyclin dependent kinase 1; CHX, cycloheximide; CQ, chloroquine; CRL4s, CUL4-RING ubiquitin ligases; DDB1, damage specific DNA binding protein 1; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; GFP, green fluorescent protein; GST, glutathione S-transferase; MAP1LC3B/LC3B, microtubule associated protein 1 light chain 3 beta; STK11/LKB1,serine/threonine kinase 11; MTORC1/MTOR complex 1, mechanistic target of rapamycin kinase complex 1; NAE1, NEDD8 activating enzyme E1 subunit 1; NOC, nocodazole; RING, really interesting new gene; RBX1, ring-box 1; SA-GLB1/ß-gal, senescence-associated galactosidase beta 1; TSC2, TSC complex subunit 2; TUBA, tubulin alpha; WIPI2, WD repeat domain, phosphoinositide interacting 2.

10.
J Comput Chem ; 40(2): 447-455, 2019 Jan 15.
Artigo em Inglês | MEDLINE | ID: mdl-30379329

RESUMO

In the present work, mechanism of the O2 (1 Δg ) generation from the reaction of the dissolved Cl2 with H2 O2 in basic aqueous solution has been explored by the combined ab initio calculation and nonadiabatic dynamics simulation, together with different solvent models. Three possible pathways have been determined for the O2 (1 Δg ) generation, but two of them are sequentially downhill processes until formation of the OOCl- complex with water, which are of high exothermic character. Once the complex is formed, singlet molecular oxygen is easily generated by its decomposition along the singlet-state pathway. However, triplet molecular oxygen of O2 ( Σ 3 g - ) can be produced with considerable probability through nonadiabatic intersystem crossing in the 1 Δg / Σ 3 g - intersection region. It has been found that the coupled solvent, heavy-atom, and nonadiabatic effects have an important influence on the quantum yield of the O2 (1 Δg ) generation. © 2018 Wiley Periodicals, Inc.

12.
Science ; 360(6385): 204-208, 2018 Apr 13.
Artigo em Inglês | MEDLINE | ID: mdl-29650672

RESUMO

Complex interactions between host immunity and the microbiome regulate norovirus infection. However, the mechanism of host immune promotion of enteric virus infection remains obscure. The cellular tropism of noroviruses is also unknown. Recently, we identified CD300lf as a murine norovirus (MNoV) receptor. In this study, we have shown that tuft cells, a rare type of intestinal epithelial cell, express CD300lf and are the target cell for MNoV in the mouse intestine. We found that type 2 cytokines, which induce tuft cell proliferation, promote MNoV infection in vivo. These cytokines can replace the effect of commensal microbiota in promoting virus infection. Our work thus provides insight into how the immune system and microbes can coordinately promote enteric viral infection.


Assuntos
Infecções por Caliciviridae/imunologia , Enterócitos/imunologia , Enterócitos/virologia , Microbiota/imunologia , Norovirus/fisiologia , Tropismo Viral/imunologia , Animais , Proliferação de Células , Citocinas/metabolismo , Camundongos , Receptores Imunológicos/metabolismo
13.
Chem Asian J ; 13(7): 780-784, 2018 Apr 04.
Artigo em Inglês | MEDLINE | ID: mdl-29446260

RESUMO

The photoresponsive azobenzene-tethered DNAs have received growing experimental attention because of their potential applications in biotechnology and nanotechnology; however, little is known about the initial photoisomerization of azobenzene in these systems. Herein we have employed quantum mechanics/molecular mechanics (QM/MM) methods to explore the photoisomerization dynamics of an azobenzene-tethered DNA duplex. We find that in the S1 state the trans-cis photoisomerization path is much steeper in DNA than in vacuo, which makes the photoisomerization much faster in the DNA environment. This acceleration is primarily caused by complex steric interactions between azobenzene and the nearby unpaired thymine nucleobase, which also change the photoisomerization mechanism of azobenzene in the DNA duplex.


Assuntos
Compostos Azo/química , DNA/química , Timina/química , Compostos Azo/efeitos da radiação , Pareamento de Bases , Isomerismo , Luz , Simulação de Dinâmica Molecular , Estrutura Molecular , Teoria Quântica
15.
J Agric Food Chem ; 66(5): 1140-1146, 2018 Feb 07.
Artigo em Inglês | MEDLINE | ID: mdl-29334729

RESUMO

Seven new polyoxygenated cyclohexenoids, namely, phomopoxides A-G (1-7), were isolated from the fermentation broth extract of an endophytic fungal strain Phomopsis sp. YE3250 from the medicinal plant Paeonia delavayi Franch. The structures of these compounds were established by spectroscopic interpretation. The absolute configurations of compounds 1 and 4 were confirmed by X-ray crystallographic analysis and chemical derivative approach. All isolated compounds showed weak cytotoxic activities toward three human tumor cell lines (Hela, MCF-7, and NCI-H460) and weak antifungal activities against five pathogenic fungi (Candida albicans, Aspergillus niger, Pyricularia oryzae, Fusarium avenaceum, and Hormodendrum compactum). In addition, compounds 1-7 showed a promising α-glycosidase inhibitory activity with IC50 values of 1.47, 1.55, 1.83, 2.76, 2.88, 3.16, and 2.94 mM, respectively, as compared with a positive control of acarbose (IC50 = 1.22 mM).


Assuntos
Ascomicetos/metabolismo , Cicloexanos/farmacologia , Inibidores Enzimáticos , Glicosídeo Hidrolases/antagonistas & inibidores , Paeonia/microbiologia , Antifúngicos , Antineoplásicos , Linhagem Celular Tumoral , Cicloexanos/química , Endófitos/metabolismo , Células HeLa , Humanos , Células MCF-7 , Oxigênio/química , Plantas Medicinais/microbiologia
16.
J Chem Phys ; 148(1): 014306, 2018 Jan 07.
Artigo em Inglês | MEDLINE | ID: mdl-29306287

RESUMO

Combining the congruence check and the first-principles calculations, we have systematically investigated the structural stabilities and gap distributions of possible diamondoids (CnHm) with the carbon numbers (n) from 10 to 41. A simple method for the nomenclature is proposed, which can be used to distinguish and screen the candidates with high efficiency. Different from previous theoretical studies, the possible diamondoids can be enumerated according to our nomenclature, without any pre-determination from experiments. The structural stabilities and electronic properties have been studied by density functional based tight binding and first-principles methods, where a nearly linear correlation is found between the energy gaps obtained by these two methods. According to the formation energy of structures, we have determined the stable configurations as a function of chemical potential. The maximum and minimum energy gaps are found to be dominated by the shape of diamondoids for clusters with a given number of carbon atoms, while the gap decreases in general as the size increases due to the quantum confinement.

17.
J Cell Mol Med ; 22(1): 439-451, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-29148232

RESUMO

Late-stage hepatocellular carcinoma (HCC) usually has a low survival rate because of the high risk of metastases and the lack of an effective cure. Disulfiram (DSF) has copper (Cu)-dependent anticancer properties in vitro and in vivo. The present work aims to explore the anti-metastasis effects and molecular mechanisms of DSF/Cu on HCC cells both in vitro and in vivo. The results showed that DSF inhibited the proliferation, migration and invasion of HCC cells. Cu improved the anti-metastatic activity of DSF, while Cu alone had no effect. Furthermore, DSF/Cu inhibited both NF-κB and TGF-ß signalling, including the nuclear translocation of NF-κB subunits and the expression of Smad4, leading to down-regulation of Snail and Slug, which contributed to phenotype epithelial-mesenchymal transition (EMT). Finally, DSF/Cu inhibited the lung metastasis of Hep3B cells not only in a subcutaneous tumour model but also in an orthotopic liver metastasis assay. These results indicated that DSF/Cu suppressed the metastasis and EMT of hepatic carcinoma through NF-κB and TGF-ß signalling. Our study indicates the potential of DSF/Cu for therapeutic use.


Assuntos
Carcinoma Hepatocelular/patologia , Cobre/farmacologia , Dissulfiram/farmacologia , Transição Epitelial-Mesenquimal/efeitos dos fármacos , Neoplasias Hepáticas/patologia , Neoplasias Pulmonares/secundário , NF-kappa B/metabolismo , Fator de Crescimento Transformador beta/metabolismo , Animais , Linhagem Celular Tumoral , Movimento Celular/efeitos dos fármacos , Regulação para Baixo/genética , Humanos , Camundongos Endogâmicos BALB C , Camundongos Nus , Invasividade Neoplásica , Fenótipo , Transdução de Sinais , Proteína Smad4/metabolismo , Fator de Crescimento Transformador beta1/farmacologia , Ensaios Antitumorais Modelo de Xenoenxerto
18.
Exp Cell Res ; 362(1): 72-82, 2018 01 01.
Artigo em Inglês | MEDLINE | ID: mdl-29155365

RESUMO

Disulfiram (DSF) in combination with copper (Cu) has been reported to override drug resistance in cancer cells, and DSF combined with chemotherapy based on the microtubule inhibitor vinorelbine appears to prolong survival in non-small cell lung cancer patients. Here, we investigated the mechanisms underlying these findings. DSF/Cu reversed the microtubule inhibitor resistance in A549/Taxol and KB/VCR cells in vitro, and had anti-tumor effects in A549/Taxol and KB/VCR xenograft mice. DSF/Cu and DSF reduced the cancer stem cell (CSC) characteristics of drug-resistant A549/Taxol and KB/VCR cells, including sphere formation, colony generation and migration, and DSF/Cu was more effective than DSF alone. DSF/Cu also decreased the aldehyde dehydrogenase (ALDH) activity and the expression of P-gp and stem cell transcription factors in A549/Taxol and KB/VCR cells. Knockdown of ALDH2 attenuated the CSC characteristics of resistant cancer cells and enhanced their sensitivity to Taxol or VCR. Importantly, DSF/Cu treatment inhibited the expression of ALDH2 in vitro and in vivo. Our findings suggest that DSF/Cu reverses microtubule inhibitor resistance in cancer cells by suppressing ALDH2 expression, and Cu improves the activity of DSF.


Assuntos
Aldeído-Desidrogenase Mitocondrial/antagonistas & inibidores , Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico , Cobre/administração & dosagem , Dissulfiram/administração & dosagem , Resistencia a Medicamentos Antineoplásicos/efeitos dos fármacos , Neoplasias Pulmonares/tratamento farmacológico , Moduladores de Tubulina/uso terapêutico , Células A549 , Animais , Carcinoma Pulmonar de Células não Pequenas/patologia , Linhagem Celular Tumoral , Sinergismo Farmacológico , Humanos , Neoplasias Pulmonares/patologia , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , Terapia de Alvo Molecular/métodos , Células-Tronco Neoplásicas/efeitos dos fármacos , Células-Tronco Neoplásicas/patologia , Ensaios Antitumorais Modelo de Xenoenxerto
19.
Oncotarget ; 8(55): 94635-94649, 2017 Nov 07.
Artigo em Inglês | MEDLINE | ID: mdl-29212255

RESUMO

Purpose: Soluble epoxide hydrolase inhibitors (sEHIs) had been demonstrated to produce cardioprotective effects against ischemia-induced lethal arrhythmias, but the exact mechanisms remain unknown. The present study was designed to investigate whether the beneficial effects of sEHIs are related to regulation of microRNA-1, which was a proarrhythmic factor in the ischemic heart. Methods: A mousemyocardial infarction (MI) model was established by ligating the coronary artery. sEHI t-AUCB (0.2, 1, 5 mg/L in drinking-water) was administered daily seven days before MI. The incidence of arrhythmias was assessed by in vivo electrophysiologic studies. miR-1, KCNJ2 (encoding the K+ channel subunit Kir2.1), and GJA1 (encoding connexin 43 [Cx43]) mRNA were measured by real-time PCR; Kir2.1 and Cx43 protein were assessed by western blotting and immunohistochemistry. Results: We demonstrated that sEHIs reduced the myocardium infarct size and incidence of inducible arrhythmias in MI mice. Up-regulation of miR-1 and down-regulation of KCNJ2/Kir2.1 and GJA1/Cx43 mRNA/protein were observed in ischemic myocaridum, whereas administration of sEHIs produced an opposite effect. In addition, miR-1 overexpression inhibited expression of the target mRNA and their corresponding proteins, whereas t-AUCB reversed the effects. Our results further revealed that PI3K/Akt signaling pathway might participate in the negatively regulation of miR-1 by sEHi. Conclusions: We conclude that sEHIs can repress miR-1, thus stimulate expression of KCNJ2/Kir2.1 and GJA1/Cx43 mRNA/protein in MI mice, suggesting a possible mechanism for its potential therapeutic application in ischemic arrhythmias.

20.
Mol Cell Oncol ; 4(6): e1364212, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-29209651

RESUMO

The tumor suppressive functions of promyelocytic leukemia (PML) have been attributed mainly to its inhibition of various malignant properties of tumor cells. Our recent work identifies a PML ubiquitination and degradation pathway, which regulates both cell and non-cell components of the tumor microenvironment, thereby potentiating immune evasion and metastasis.

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