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Moisture content testing of agricultural products is critical for quality control, processing efficiency and storage management. Testing foxtail millet moisture content ensures stable foxtail millet quality and helps farmers determine the best time to harvest. A differential capacitance moisture content detection device was designed based on STM32 and PCAP01 capacitance digital converter chip. The capacitance method combined with the back-propagation(BP) algorithm and the extreme learning machine(ELM) algorithm was chosen to construct an analytical model for foxtail millet moisture content, temperature, and volume duty cycle. This work performs capacitance measurements on foxtail millet with different moisture contents, temperatures, and proportions of the measured substance occupying the detection area (that is, the volumetric duty cycle). On this foundation, the sparrow search algorithm (SSA) is used to optimize the BP and ELM models. However, SSA may encounter problems such as falling into local optimization solutions due to the reduction of population diversity in the late iterations. As a consequence, Logistic algorithm is introduced to optimize SSA, making it more appropriate for solving specific problems. Upon comparative analysis, the model predicted using the Logistic-SSA-ELM algorithm was more accurate. The results indicate that the predicted values of prediction set coefficient of determination (RP), prediction set root mean square error (RMSEP) and prediction set ratio performance deviation (RPDP) were 0.7016, 3.7150 and 1.4035, respectively. This algorithm has excellent prediction performance and can be used as a model for detection of foxtail millet moisture content. In view of the important role of foxtail millet moisture content detection in acquisition and storage, it is particularly important to study a nondestructive and fast online real-time detection method. The designed capacitive sensor with differential structure has well stabilization and high accuracy, which can be further studied in depth and gradually move towards the general trend of agricultural development of smart agriculture and precision agriculture.
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OBJECTIVE: This study aimed to explore the key alternative splicing events in costimulatory molecule-related genes in colon cancer and to determine their correlation with prognosis. METHODS: Gene expression RNA-sequencing data, clinical data, and SpliceSeq data of colon cancer were obtained from The Cancer Genome Atlas. Differentially expressed alternative splicing events in genes were identified, Followed by correlation analysis of genes corresponding to differentially expressed alternative splicing events with costimulatory molecule-related genes. Survival analysis was conducted using differentially expressed alternative splicing events in these genes and a prognostic model was constructed. Functional enrichment, proteinprotein interaction network, and splicing factor analyses were performed. RESULTS: In total, 6504 differentially expressed alternative splicing events in 3949 genes were identified between tumor and normal tissues. Correlation analysis revealed 3499 differentially expressed alternative splicing events in 2168 costimulatory molecule-related genes. Moreover, 328 differentially expressed alternative splicing events in 288 costimulatory molecule-related genes were associated with overall survival. The prognostic models constructed using these showed considerable power in predicting survival. The ubiquitin A-52 residue ribosomal protein fusion product 1 and ribosomal protein S9 were the hub nodes in the protein-protein interaction network. Furthermore, one splicing factor, splicing factor proline and glutamine-rich, was significantly associated with patient prognosis. Four splicing factor-alternative splicing pairs were obtained from four alternative splicing events in three genes: TBC1 domain family member 8 B, complement factor H, and mitochondrial fission 1. CONCLUSION: The identified differentially expressed alternative splicing events of costimulatory molecule-related genes may be used to predict patient prognosis and immunotherapy responses in colon cancer.
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OBJECTIVES: Sleep and psychological disorders are common complaints in stroke survivors. The effectiveness of sleep duration in post-stroke on mental well-being and health outcomes has been reported recently. This study aimed to investigate the mediating effect of sleep duration on the relationship between anxiety and health-related quality of life in Chinese post-stroke; MATERIALS AND METHODS: We conducted a quantitative, cross-sectional study with participants recruited through a multistage, stratified, probability proportional to size sampling method. Anxiety, health-related quality of life, and sleep duration were measured by Zung Self-rating Anxiety Scale, World Health Organization Quality of Life Questionnaire, and a self-administered, structured questionnaire. A multiple linear regression analysis was conducted to identify the association between anxiety, sleep duration, and quality of life. The direct and indirect effects of sleep duration on health-related quality of life was assessed using the bootstrap method via Model 4 (parallel mediation) of SPSS PROCESS macro; RESULTS: A total of 856 post-stroke patients participated in the study, and incidence of anxiety symptom amongst post-stroke was 33.53%. Sleep duration mainly plays partial mediating roles in the relationship between mild-to-moderate anxiety and quality of life in physical, psychological, and environment domains, with sleep duration of 7-8h playing a major role; CONCLUSIONS: A significant relationship among anxiety, sleep duration, and quality of life in post-stroke was found in this study. The sleep duration partially mediated the association between anxiety and quality of life. Suitable prevention methods and early interventions for sleep duration may improve the quality of life for post-stroke anxiety.
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We demonstrated here an efficient synthetic method of carbazole derivatives from readily available N-arylnaphthalen-2-amines and quinone esters catalyzed by Brønsted acid. With this strategy, a series of carbazole derivatives were obtained in good to excellent yields (76 to >99) under mild conditions. Large scale reaction illustrated the synthetic utility of this protocol. Meanwhile, a series of C-N axially chiral carbazole derivatives were also constructed in moderate to good yields (36-89% yield) with moderate to excellent atroposelectivities (44-94% ee) by using chiral phosphoric acid as a catalyst, which provides a novel strategy for the atroposelective construction of C-N axially chiral compounds and a new member of the C-N atropisomers.
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Strong ultraviolet (UV) radiation at high altitude imposes a serious selective pressure, which may induce skin pigmentation adaptation of indigenous populations. We conducted skin pigmentation phenotyping and genome-wide analysis of Tibetans in order to understand the underlying mechanism of adaptation to UV radiation. We observe that Tibetans have darker baseline skin color compared with lowland Han Chinese, as well as an improved tanning ability, suggesting a two-level adaptation to boost their melanin production. A genome-wide search for the responsible genes identifies GNPAT showing strong signals of positive selection in Tibetans. An enhancer mutation (rs75356281) located in GNPAT intron 2 is enriched in Tibetans (58%) but rare in other world populations (0 to 18%). The adaptive allele of rs75356281 is associated with darker skin in Tibetans and, under UVB treatment, it displays higher enhancer activities compared with the wild-type allele in in vitro luciferase assays. Transcriptome analyses of gene-edited cells clearly show that with UVB treatment, the adaptive variant of GNPAT promotes melanin synthesis, likely through the interactions of CAT and ACAA1 in peroxisomes with other pigmentation genes, and they act synergistically, leading to an improved tanning ability in Tibetans for UV protection.
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Adaptação Fisiológica , Altitude , Pigmentação da Pele , Aciltransferases/genética , Adaptação Fisiológica/genética , Etnicidade , Humanos , Melaninas/genética , Fenótipo , Pigmentação da Pele/genética , Tibet , Transcriptoma , Raios UltravioletaRESUMO
Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder whose pathogenesis is still unclear. MicroRNAs (miRNAs) are a kind of endogenous small non-coding RNAs that play important roles in the post-transcriptional regulation of genes. Recent researches show that miRNAs are edited in multiple ways especially in central nervous systems. A-to-I editing of RNA catalyzed by Adenosine deaminases acting on RNA (ADARs) happens intensively in brain and is also noticed in other organs and tissues. Although miRNAs are widely edited in human brain, miRNA editing in ASD is still largely unexplored. In order to reveal the editing events of miRNAs in ASD, we analyzed 131 miRNA-seq samples from 8 different brain regions of ASD patients and normal controls. We identified 834 editing sites with significant editing levels, of which 70 sites showed significantly different editing levels in the superior frontal gyrus samples of ASD patients (ASD-SFG) when compared with those of control samples. The editing level of an A-to-I editing site in hsa-mir-376a-1 (hsa-mir-376a-1_9_A_g) in ASD-SFG is higher than that of normal controls, and the difference is exaggerated in individuals under 10 years. The increased expression of ADAR1 is consistent with the increased editing level of hsa-mir-376a-1_9_A_g in ASD-SFG samples compared to normal SFG samples. Furthermore, we verify that A-to-I edited hsa-mir-376a-5p directly represses GPR85 and NAPB, which may contribute to the abnormal neuronal development of ASD patients. These results provide new insights into the mechanism of ASD.
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OBJECTIVE: Increasing evidence has indicated an association between gut microbiota in gastrointestinal cancer and clinical outcome. Herein, we aim to develop a prognosis-prediction tool based on an immune-lipid metabolism signature, tumor cell-associated immune microenvironment, and lipid metabolism proteins inferred from the function of gut microbiota. METHODS: 16S gene ribosomal RNA sequencing was performed on 10 fecal samples obtained after tumor resection but before chemotherapy (EBVaGC = 4 and EBVnGC = 6). Least absolute shrinkage and selection operator (LASSO) Cox regression was applied to screening for highly accurate marker proteins. A compound score based on the fraction of screened markers was then constructed using a LASSO logistic regression model. RESULTS: The Tax4Fun analysis based on Kyoto Encyclopedia of Genes and Genomes data indicated differentially expressed tumor pathway between EBVnGC and EBVaGC. Using the LASSO logistic model, a compound score was established consisting of 14 types of immune microenvironment and lipid metabolism proteins. In the training set (378 patients), significant differences were found between high- and low-compound score groups in overall survival across and within subpopulations with an identical EBV. Multivariable analysis revealed that the compound score was an independent prognostic factor (hazard ratio, 2.26; 95% confidence interval = 2.28-3.36). The prognostic value ;of the compound score was also confirmed in the validation (162 patients) and entire (540 patients) sets. DISCUSSION: The proposed compound score is a promising signature for estimating overall survival in patients with gastric cancer having EBVaGCs or EBVnGCs.
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Adenocarcinoma/mortalidade , Biomarcadores Tumorais/análise , Infecções por Vírus Epstein-Barr/mortalidade , Microbioma Gastrointestinal/imunologia , Neoplasias Gástricas/mortalidade , Adenocarcinoma/imunologia , Adenocarcinoma/microbiologia , Adenocarcinoma/terapia , Biomarcadores Tumorais/imunologia , Biomarcadores Tumorais/metabolismo , Quimioterapia Adjuvante , DNA Bacteriano/isolamento & purificação , Infecções por Vírus Epstein-Barr/imunologia , Infecções por Vírus Epstein-Barr/microbiologia , Infecções por Vírus Epstein-Barr/terapia , Estudos de Viabilidade , Fezes/microbiologia , Feminino , Seguimentos , Gastrectomia , Microbioma Gastrointestinal/genética , Herpesvirus Humano 4/imunologia , Herpesvirus Humano 4/isolamento & purificação , Humanos , Estimativa de Kaplan-Meier , Metabolismo dos Lipídeos/imunologia , Masculino , Pessoa de Meia-Idade , Projetos Piloto , Valor Preditivo dos Testes , Prognóstico , RNA Ribossômico 16S/genética , Análise de Regressão , Estudos Retrospectivos , Estômago/microbiologia , Estômago/cirurgia , Neoplasias Gástricas/imunologia , Neoplasias Gástricas/microbiologia , Neoplasias Gástricas/terapia , Microambiente Tumoral/imunologiaRESUMO
The diffusion coatings were deposited on commercially pure Ti and Ti-6Al-4V alloy at up to 1000 °C for up to 10 h using the pack cementation method. The pack powders consisted of 4 wt% Al (Al reservoir) and 4 wt% NH4Cl (activator) which were balanced with Al2O3 (inert filler). The growth kinetics of coatings were gravimetrically measured by a high precision balance. The aluminised specimens were characterised by means of scanning electron microscopy (SEM), energy dispersive spectrometer (EDS) and X-ray diffraction (XRD). At the early stages of deposition, a TiO2 (rutile) scale, other than aluminide coating, was developed on both materials at <900 °C. As the experimental temperature arose above 900 °C, the rutile layer became unstable and reduced to the low oxidation state of Ti oxides. When the temperature increased to 1000 °C, the TiO2 scale dissociated almost completely and the aluminide coating began to develop. After a triple-layered coating was generated, the coating growth was governed by the outward migration of Ti species from the substrates and obeyed the parabolic law. The coating formed consisted of an outer layer of Al3Ti, a mid-layer of Al2Ti and an inner layer of AlTi. The outer layer of Al3Ti dominated the thickness of the aluminide coating.
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The corrosion behavior of zinc-rich epoxy primers or paints (ZRPs) with different conducting polyaniline-grafted graphene (PANI/Gr) contents was investigated. Conductivity of the formed PANI/Gr nanosheets was significantly improved by employing the Gr as the inner template to synthesize the PANI. The protective properties and electrochemical behavior of coatings with artificial defects were investigated by monitoring the free corrosion potential versus time and by using localized electrochemical impedance spectroscopy (LEIS). A synergetic enhancement of the physical barrier role of the coating and the zinc sacrificial cathodic protection was achieved in the case of ZRP including PANI/Gr nanosheets. In addition, the ZRP mixed with the PANI/Gr at a content of 0.6% exhibited the best anticorrosion performance across the range of investigated PANI/Gr contents.
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Recent study has reported that microRNA-628-5p (miR-628-5p) is involved in the development of epithelial ovarian cancer; however, the mechanisms of miR-628-5p in glioma remain unclear. In this study, we explored the potential biological roles of miR-628-5p in glioma. First, we found that miR-628-5p was decreased in the tissues and cells (U87 and T98) of glioma. Second, overexpressing miR-628-5p reduced the ability of glioma cells' proliferation and induced glioma cells' cycle arrest in G1. Then, we found that miR-628-5p directly bound to the 3'-untranslated region of DDX59 and decreased the protein level of DDX59. The decrease of DDX59 was found to lead to the decrease of p-AKT. Mechanistic studies revealed that restoring the expression of DDX59 alleviated miR-628-5p-induced inhibition of proliferation of glioma. These findings suggest that the miR-628-5p/DDX59 axis has a key role in the development of glioma, and miR-628-5p might be a new therapeutic target against glioma.
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Biomarcadores Tumorais/metabolismo , Neoplasias Encefálicas/patologia , Proliferação de Células , Regulação Neoplásica da Expressão Gênica , Glioma/patologia , MicroRNAs/genética , RNA Helicases/metabolismo , Animais , Apoptose , Biomarcadores Tumorais/genética , Neoplasias Encefálicas/genética , Neoplasias Encefálicas/metabolismo , Ciclo Celular , Glioma/genética , Glioma/metabolismo , Humanos , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , Prognóstico , RNA Helicases/genética , Células Tumorais Cultivadas , Ensaios Antitumorais Modelo de XenoenxertoRESUMO
AIM: To investigate the expression and clinical significance of B7 homolog 3 (B7-H3) and ß-1,3-galactosyltransferase-4 (B3GALT4) in colorectal cancer (CRC) patients. METHODS: Using tissue microarray, we identified the expression of B7-H3 and B3GALT4 in 223 CRC patient samples by immunohistochemistry and evaluated the possible correlation between B7-H3 and B3GALT4 and clinical outcomes. Further, the mRNA and protein expression were identified to establish the regulatory relationship of B7-H3 with B3GALT4 in vitro. RESULTS: A significant positive correlation between B7-H3 and B3GALT4 was observed in CRC specimens (r = 0.219, P = 0.001). High expression of B7-H3 was identified as a significant independent predictor of poor overall survival (OS) [hazard ratio (HR) = 1.781; 95%CI: 1.027-3.089; P = 0.040]. Moreover, high expression of B3GALT4 was also recognized as an independent predictor of inferior OS (HR = 1.597; 95%CI: 1.007-2.533; P = 0.047). Additionally, CRC patients expressing both high B7-H3 and high B3GALT4 contributed to a significant decrease in OS (HR = 2.283; 95%CI: 1.289-4.042; P = 0.005). In CRC cell lines with stable expression of high B7-H3, the mRNA and protein expressions of B3GALT4 were significantly upregulated. Similarly, the expression of B3GALT4 was significantly reduced when expression of B7-H3 was knocked down. CONCLUSION: The expression of B3GALT4 in CRC is positively correlated with B7-H3 expression in vitro. B7-H3/B3GLAT4 may be used as dual prognostic biomarkers for CRC.
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Antígenos B7/metabolismo , Biomarcadores Tumorais/metabolismo , Neoplasias Colorretais/patologia , Galactosiltransferases/metabolismo , Antígenos B7/genética , Linhagem Celular Tumoral , Neoplasias Colorretais/mortalidade , Neoplasias Colorretais/cirurgia , Feminino , Seguimentos , Regulação Neoplásica da Expressão Gênica , Técnicas de Silenciamento de Genes , Humanos , Imuno-Histoquímica , Estimativa de Kaplan-Meier , Masculino , Pessoa de Meia-Idade , Prognóstico , RNA Mensageiro/metabolismo , Análise Serial de Tecidos , Regulação para CimaRESUMO
BACKGROUND: Hyperglycemia is associated with dismal outcomes in patients with traumatic brain injury (TBI), which is frequently treated with insulin therapy. In this study, a systematic review and meta-analysis of the published randomized controlled trials (RCTs) was performed to assess the safety and efficacy of intensive glycemic control (IGC) versus conventional glycemic control (CGC) for patients following TBI. METHODS: Databases, including PubMed, Embase, and the Cochran database, were retrieved up to January 2018. The outcomes evaluated in this study included mortality, neurological outcome, infection rate, hypoglycemia episode, and length of stay (LOS) in intensive care unit (ICU). The enrolled trials were analyzed using the Review Manager 5.3 software. RESULTS: A total of 7 randomized controlled trials (RCTs) involving 1013 cases were enrolled in this study, and the results indicated no significant difference in 6-month mortality (risk ratio [RR], 0.92; 95% confidence interval [CI] 0.76-1.10; Pâ=â.34). Subsequently, IGC was associated with a better neurological outcome (RR, 1.22; 95% CI 1.05-1.43; Pâ=â.01), lower infection rate (RR, 0.65; 95% CI 0.51-0.82; Pâ=â.0003) and shorter LOS in ICU (mean difference [MD]â=â-1.37; 95%CIâ=â-2.11, -0.63; Pâ=â.0003). In addition, IGC would also increase the risk of hypoglycemia episode (RR, 4.53; 95% CI 2.18-9.42; Pâ<â.001). CONCLUSIONS: IGC plays a protective role in improving neurological outcome, decreasing infection rate and reducing the LOS in ICU. However, IGC therapy can also remarkably increase the risk of hypoglycemia, but it will not affect the mortality in TBI patients.
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Lesões Encefálicas Traumáticas/complicações , Hiperglicemia/tratamento farmacológico , Hipoglicemiantes/uso terapêutico , Insulina/uso terapêutico , Lesões Encefálicas Traumáticas/mortalidade , Cuidados Críticos , Humanos , Hiperglicemia/etiologia , Hipoglicemia/induzido quimicamente , Hipoglicemiantes/efeitos adversos , Controle de Infecções , Infecções/etiologia , Insulina/efeitos adversos , Tempo de Internação , Prognóstico , Ensaios Clínicos Controlados Aleatórios como Assunto , Fatores de RiscoRESUMO
Acyl-CoA thioesterase 1 (ACOT1) is an important isoform of the ACOT family that catalyzes the reaction of fatty acyl-CoAs to CoA-SH and free fatty acids. Recent studies of gastrointestinal tumor metabolism suggest that there is abnormal metabolism of lipids and fatty acids during tumor progression. However, the function and contribution of ACOT1 in gastric cancer development are still poorly understood. In addition, GLI3 is a major transcription factor in the regulation of hedgehog signaling. GLI3 mutations induce glandular expansion and intestinal metaplasia in gastric cancer, which indicates a role for GLI3 in the preneoplastic process. Thus, we investigated the relationship between ACOT1 expression and GLI3 in gastric adenocarcinoma. A tissue microarray was constructed from 280 cases of gastric adenocarcinoma. The immunohistochemistry method was performed on tissue sections of 4 µm from each tissue microarray block. We found a significant correlation between ACOT1 expression and poor histologic grade, a lower T category, TNM stage, and increased GLI3 expression. In addition, the survival analysis revealed that the ACOT1-positive group had significantly decreased overall survival rates compared with the ACOT1-negative group. Furthermore, GLI3 expression had a significant positive correlation with ACOT1 expression in gastric adenocarcinoma cells. In summary, these findings demonstrate that increased expression of ACOT1 is correlated with pivotal clinicopathological parameters and poor prognosis in gastric adenocarcinoma through increased expression of the potential tumor-promoting protein GLI3.
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Adenocarcinoma/metabolismo , Proteínas do Tecido Nervoso/genética , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/mortalidade , Tioléster Hidrolases/metabolismo , Proteína Gli3 com Dedos de Zinco/genética , Adenocarcinoma/genética , Adenocarcinoma/mortalidade , Adulto , Idoso , Idoso de 80 Anos ou mais , Feminino , Humanos , Imuno-Histoquímica/métodos , Masculino , Pessoa de Meia-Idade , Prognóstico , Transdução de Sinais/fisiologia , Neoplasias Gástricas/genética , Taxa de SobrevidaRESUMO
Jab1 (Jun activation domain-binding protein 1), also known as CSN5 (COP9 signalosome subunit 5), is frequently overexpressed in several cancer types. However, the biological functions and the molecular mechanisms of the Jab1 protein in human gliomas have not been investigated. In this study, we found that Jab1 protein was increasingly expressed in human glioma tissues comparing with normal brain tissues (Non-tumor). This suggested that Jab1 might be involved in the development of glioma. Thus, the role of Jab1 in glioma cell proliferation was investigated using Jab1 loss- and gain-of-function. The results showed that downregulation of Jab1 significantly inhibited glioma cell proliferation, while overexpression of Jab1 promoted it. Further investigation on molecular targets revealed that silencing of Jab1 obviously increased the p53 protein level thereby promoting the transcription of ubiquitin ligase Siah1 (Seven in absentia homolog 1), which aggravates the degradation of ß-catenin. In contrast, overexpression of Jab1 had the opposite effect. Taken together, these findings suggest that Jab1 promotes glioma cell proliferation and increased expression of Jab1 in glioma patients may amplify ß-catenin signaling to contribute to glioma cell proliferation.
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Neoplasias Encefálicas/patologia , Complexo do Signalossomo COP9/metabolismo , Proliferação de Células/fisiologia , Regulação Neoplásica da Expressão Gênica/fisiologia , Glioma/patologia , Peptídeos e Proteínas de Sinalização Intracelular/metabolismo , Proteínas Nucleares/metabolismo , Peptídeo Hidrolases/metabolismo , Transdução de Sinais/efeitos dos fármacos , Ubiquitina-Proteína Ligases/metabolismo , beta Catenina/metabolismo , Análise de Variância , Complexo do Signalossomo COP9/genética , Linhagem Celular Tumoral/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Ensaio de Unidades Formadoras de Colônias , Feminino , Proteínas de Fluorescência Verde/genética , Proteínas de Fluorescência Verde/metabolismo , Humanos , Peptídeos e Proteínas de Sinalização Intracelular/genética , Masculino , Proteínas Nucleares/genética , Peptídeo Hidrolases/genética , RNA Interferente Pequeno/genética , RNA Interferente Pequeno/metabolismo , Transfecção , Ubiquitina-Proteína Ligases/genética , Ureia/análogos & derivados , Ureia/farmacologia , beta Catenina/genéticaRESUMO
Hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC) is the most widespread type of liver cancer. However, the underlying mechanism of HCC tumorigenesis is very intricate and HBV-encoded X protein (HBx) has been reported to play a key role in this process. It has been reported that HBx up-regulates the transcription of ErbB3. However, it remains unclear whether HBx can regulate ErbB3 expression at post-translational modification level. In this study, we showed that HBx interacts with ubiquitin ligase Nrdp1 (neuregulin receptor degradation protein 1) and decreases its stability, which results in the up-regulation of ErbB3 and promotion of HCC cells. Moreover, the expression of ErbB3 was almost undetectable in normal liver tissues but was relative abundant in HCC tissues, and the level of ErbB3 and Nrdp1 significantly showed a negative correlation in HCC tissues. Taken together, these findings suggest that HBx promotes the progression of HCC by decreasing the stability of Nrdp1, which results in up-regulation of ErbB3, suggesting that ErbB3 may be a target for HCC therapy.
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Carcinoma Hepatocelular/virologia , Regulação Neoplásica da Expressão Gênica/fisiologia , Neoplasias Hepáticas/virologia , Receptor ErbB-3/biossíntese , Transativadores/metabolismo , Ubiquitina-Proteína Ligases/metabolismo , Western Blotting , Carcinoma Hepatocelular/metabolismo , Carcinoma Hepatocelular/patologia , Transformação Celular Viral/fisiologia , Imunofluorescência , Hepatite B/complicações , Humanos , Imuno-Histoquímica , Imunoprecipitação , Neoplasias Hepáticas/metabolismo , Neoplasias Hepáticas/patologia , Regulação para Cima , Proteínas Virais Reguladoras e AcessóriasRESUMO
Calcyclin-binding protein or Siah-1-interacting protein (CacyBP/SIP) was previously reported to promote the proliferation of glioma cells. However, the effect of CacyBP/SIP on apoptosis of glioma is poorly understood. Here, our study shows that CacyBP/SIP plays a role in inhibiting doxorubicin (DOX) induced apoptosis of glioma cells U251 and U87. Overexpression of CacyBP/SIP obviously suppressed the DOX-induced cell apoptosis. On the contrary, silencing of CacyBP/SIP significantly promoted it. Further investigation indicated that inhibition of apoptosis by CacyBP/SIP was relevant to its nuclear translocation in response to the DOX treatment. Importantly, we found that the level of p-ERK1/2 in nuclei was related to the nuclear accumulation of CacyBP/SIP. Finally, the role of CacyBP/SIP was confirmed in vivo in a mouse model with the cell line stably silencing CacyBP/SIP. Taken together, our results suggest that CacyBP/SIP plays an important role in inhibiting apoptosis of glioma cells which might be mediated by ERK1/2 signaling pathway, which will provide some guidance for the treatment of glioma.