RESUMO
The purpose of this study was to investigate the effect of sunflower kernel peptides produced by enzymatic digestion, fermentation, or both on the growth performance, nutrient digestibility, and health status of broilers. Four diets contained 20% of sunflower kernel meal as its raw form (CON) or degraded by protease (ESM), Bacillus pumilus (FSM), or both (DSM). A total of 480 yellow broilers at one day old were randomly distributed to 4 groups with 6 replicates of 20 chicks each. The feeding trial lasted for 63 d. Results showed that peptide content was increased (p<0.001) from 3.97% (CON) to 32.5% (ESM), 24.2% (FSM), and 39.1% (DSM). The three sunflower peptide groups improved (p≤0.001) feed intake and body weight gain. The peptide groups increased (p≤0.015) ileal apparent digestibility of dry matter, energy, crude protein, and amino acids (methionine, lysine, tryptophan, and threonine). Furthermore, the peptide groups improved (p≤0.029) the health status by increasing serum immunoglobulins (IgA, IgG) and glutathione peroxidase. Additionally, among the peptide groups, DSM showed more pronounced effects (p<0.05) on these parameters than ESM or FSM. It is concluded that dual-degradation by enzymolysis and fermentation has a better improvement in the nutrition and application of sunflower kernel meal in broilers.(AU)
Assuntos
Animais , Peptídeos/efeitos adversos , Galinhas/fisiologia , Fenômenos Fisiológicos da Nutrição Animal , Helianthus/química , Valor NutritivoRESUMO
PURPOSE: Anaplastic thyroid carcinoma (ATC) is one of the most aggressive cancers in the world. Stearoyl-CoA desaturase-1 (SCD-1) is one of major enzymes in the de novo synthesis of fatty acids and is related to cancer aggressiveness and poor patient prognosis. The study aimed to construct exosomes loaded SCD-1 interference, investigate its effects and mechanisms on the cell proliferation and apoptosis of ATC cells. METHODS: The expressions of SCD-1 in normal thyroid cell line and ATC cell lines were determined by qRT-PCR and western blotting, respectively. Exosomes were prepared and purification then loaded with SCD-1 siRNA by electroporation and observed by transmission electron microscopy. Higher SCD-1 mRNA and protein levels were found in ATC cell lines compared than normal thyroid cell line (P < 0.05), and both Hth-7 and FRO cells could uptake PKH67-labeled exosomes. The effects of exosomes loaded SCD-1 siRNA on ATC cells were measured by CCK8 assay and apoptosis detection kit. RESULTS: When compared with control group, the cell viability significantly decreased in both two ATC cell lines taken up exosomes loaded SCD-1 siRNA (P < 0.001), and apoptotic and necrotic cells obviously increased (P < 0.05). In order to explore the mechanism of exosomes loaded SCD-1 on ATC, the ROS level was detected by fluorescence reagent. It was found that exosomes loaded SCD-1 siRNA significantly increased intracellular ROS level of ATC cells (P < 0.05). CONCLUSIONS: Exosomes loaded SCD-1 siRNA inhibited ATC cellular proliferation and promoted cellular apoptosis, and the mechanisms involved maybe the regulation of fatty acids metabolism and ROS level. Our study provides a promising therapeutic strategy for ATC.
Assuntos
Exossomos/fisiologia , RNA Interferente Pequeno/fisiologia , Estearoil-CoA Dessaturase/metabolismo , Carcinoma Anaplásico da Tireoide/patologia , Neoplasias da Glândula Tireoide/patologia , Apoptose , Proliferação de Células , Humanos , Células Tumorais CultivadasRESUMO
Chicken coccidiosis is a common and severe parasitic disease caused by infection from Eimeria spp., which affects the integrity of the intestinal mucosa. TGF-ß has been shown to play an important role in the healing of intestinal mucosas, immunity, and the maintenance of bowel mucosa integrity. Very little is known about the presence of the components of TGF-ß/Smads signaling pathway of chicken at different times following coccidian infection. In the present study, we measured the levels of TGF-ß2, 3, 4, receptor TßRI, II, down-stream Smad 2, 3, 7 in cecum and spleen of chicken at different times after inoculation with Eimeria tenella using quantitative real-time PCR. The results showed that the TGF-ß/Smads signaling pathway was not activated in cecum in the early stage of infection. However, on the 8th day, the expression of TGF-ß2, 4, down-stream protein Smad 2, 7 were significant up-regulated in the spleen, which indicated that the TGF-ß/Smads signaling was changed in the E. tenella infection and was differentially expressed in various tissues in the early stages of infection.(AU)
Assuntos
Animais , Feminino , Doenças das Aves Domésticas/microbiologia , Galinhas/microbiologia , Fator de Crescimento Transformador beta/análise , Eimeria tenella/enzimologia , Coccidiose/veterinária , Baço/microbiologia , Inoculações Seriadas/veterinária , Expressão Gênica/fisiologia , Ceco/microbiologia , Reação em Cadeia da Polimerase em Tempo Real/métodos , Mucosa IntestinalRESUMO
Chicken abdominal fat (AF) is an economically important trait, and many studies have been conducted on genetic selection for AF. However, previous studies have focused on detecting functional chromosome mutations or regions using gene chips. The present study used the specific-locus amplified fragment sequencing (SLAF-seq) technology to perform a genome-wide association study (GWAS) on purebred Wengshang Barred chicken. A total of 1,286,715 single-nucleotide polymorphisms (SNPs) were detected, and 175,211 SNPs were selected as candidate SNPs for genome-wide association analysis using TASSEL general linear models. Two SNPs markers reached genome-wide significance. Of these, rs7943847, rs127627362 were significantly associated with AF at 120 days. These SNPs are close to eight genes (SLC16A6, ARSG, WIPI1, PRKAR1A, FAM20A, ABCA8, ABCA9, CPQ,). These results would enrich the studies on AF and promote the use of Chinese chicken, especially the Wenshang Barred chicken.(AU)
Assuntos
Animais , Seleção Genética/fisiologia , Galinhas/genética , Polimorfismo Genético , Gordura Abdominal/fisiologiaRESUMO
This study aimed to investigate the effect of tetramethylpyrazine (TMP) supplementation on egg production, nutrient retention and cecal microbiota diversity using 288 commercial Hy-Line brown hens as of wk 75 to 86. Four treatments consisted of TMP addition at 0 (control, basal diet), 100, 150 and 200 mg/kg of diet. The results showed that diets supplemented with TMP addition improved egg-laying rate as of wk 77 compared to the control, which led to an increase (p<0.001) of egg mass by 97-225 g/hen throughout the whole trial, and a linear increase (p=0.003) of egg mass to the incremental TMP doses was found. At wk 86, the apparent digestibilities of dry matter and crude protein were enhanced (p<0.05), exhibiting consistent linear increases (p≤0.033) with the TMP doses. However, TMP did not cause alpha and beta diversity of cecal microbiota. The results suggest that TMP can be an additive to improve egg production and nutrient digestibility of aged laying hens.(AU)
Assuntos
Animais , Pirazinas/efeitos adversos , Galinhas/fisiologia , Suplementos Nutricionais/análise , Microbioma Gastrointestinal/fisiologia , Biodiversidade , Ovos/análiseRESUMO
BACKGROUND: There is currently no formal consensus on the administration of adjuvant chemotherapy to stage I lung squamous cell carcinoma (LUSC) patients despite the poor prognosis. The side effects of adjuvant chemotherapy need to be balanced against the risk of tumour recurrence. Prognostic markers are thus needed to identify those at higher risks and recommend individualised treatment regimens. METHODS: Clinical and sequencing data of stage I patients were retrieved from the Lung Squamous Cell Carcinoma project of the Cancer Genome Atlas (TCGA) and three tissue microarray datasets. In a novel K-resample gene selection algorithm, gene-wise Cox proportional hazard regressions were repeated for 50 iterations with random resamples from the TCGA training dataset. The top 200 genes with the best predictive power for survival were chosen to undergo an L1-penalised Cox regression for further gene selection. RESULTS: A total of 602 samples of LUSC were included, of which 42.2% came from female patients, 45.3% were stage IA cancer. From an initial pool of 11,212 genes in the TCGA training dataset, a final set of 12 genes were selected to construct the multivariate Cox prognostic model. Among the 12 selected genes, 5 genes, STAU1, ADGRF1, ATF7IP2, MALL and KRT23, were adverse prognostic factors for patients, while seven genes, NDUFB1, CNPY2, ZNF394, PIN4, FZD8, NBPF26 and EPYC, were positive prognostic factors. An equation for risk score was thus constructed from the final multivariate Cox model. The model performance was tested in the sequestered TCGA testing dataset and validated in external tissue microarray datasets (GSE4573, GSE31210 and GSE50081), demonstrating its efficacy in stratifying patients into high- and low-risk groups with significant survival difference both in the whole set (including stage IA and IB) and in the stage IA only subgroup of each set. The prognostic power remains significant after adjusting for standard clinical factors. When benchmarked against other prominent gene-signature based prognostic models, the model outperformed the rest in the TCGA testing dataset and in predicting long-term risk at eight years in all three validation datasets. CONCLUSION: The 12-gene prognostic model may serve as a useful complementary clinical risk-stratification tool for stage I and especially stage IA lung squamous cell carcinoma patients to guide clinical decision making.
Assuntos
Carcinoma de Células Escamosas/genética , Perfilação da Expressão Gênica , Neoplasias Pulmonares/genética , Recidiva Local de Neoplasia/genética , Transcriptoma , Idoso , Idoso de 80 Anos ou mais , Benchmarking , Carcinoma Pulmonar de Células não Pequenas/genética , Carcinoma de Células Escamosas/tratamento farmacológico , Carcinoma de Células Escamosas/mortalidade , Carcinoma de Células Escamosas/patologia , Quimioterapia Adjuvante/efeitos adversos , Feminino , Humanos , Neoplasias Pulmonares/tratamento farmacológico , Neoplasias Pulmonares/mortalidade , Neoplasias Pulmonares/patologia , Masculino , Pessoa de Meia-Idade , Estadiamento de Neoplasias , Prognóstico , Modelos de Riscos Proporcionais , Estudos Retrospectivos , Carga TumoralRESUMO
PURPOSE: PIM kinase is called proto-oncogene, but there are less research on PIM family in colon cancer. This study was designed to explore the prognosis of PIM3 in colon cancer. METHODS: In this study, we downloaded RNA-seq and clinical information of colon cancer from the Gene Expression Omnibus (GEO) database. Kaplan-Meier method was used for analyzing the impact of PIM3 on the survival of patients with colon cancer. Single-factor and multi-factor cox regression analysis were used for verifying the prognostic value of PIM3. Spearman correlation analysis was used for screening PIM3 related genes. Functional enrichment analysis was used for analyzing the biological functions and pathways in which PIM3 related genes may be involved. STRING online tools were used for building a co-expression network. Cytoscape was used for co-expression network visualization. RESULTS: Compared with the low expression group, the patients in the PIM3 high expression group lived longer time. Single-factor and multi-factor cox regression analysis indicated that PIM3 was an independent prognostic factor for colon cancer. Sixty-two PIM3 related genes were screened, and GO and KEGG enrichment analyses suggested that PIM3 related genes might be involved in the MAPK and WNT pathways. The co-expression network showed a strong correlation between PIM3 and MLKL, MYL5, PPP3R1 and other genes. CONCLUSIONS: PIM3 is an independent prognostic factor of colon cancer and may be a target for the diagnosis and treatment of colon cancer.
Assuntos
Neoplasias do Colo/genética , Neoplasias do Colo/mortalidade , Perfilação da Expressão Gênica , Proteínas Serina-Treonina Quinases/genética , Proteínas Proto-Oncogênicas/genética , Calcineurina/genética , Neoplasias do Colo/patologia , Bases de Dados Genéticas , Humanos , Estimativa de Kaplan-Meier , Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo , Prognóstico , Proteína da Leucemia Promielocítica/genética , Proteínas Quinases/genética , Proteínas Serina-Treonina Quinases/fisiologia , Proteínas Proto-Oncogênicas/fisiologia , Análise de Regressão , Via de Sinalização WntRESUMO
PURPOSE: This paper aims to observe the expressions of VEGF and MMP-2 in patients with nasopharyngeal carcinoma treated by nimotuzumab combined with cisplatin. METHODS: Altogether, 104 patients with nasopharyngeal carcinoma treated in our hospital from April 2014 to August 2016 were selected as research subjects. Among them, 50 patients treated with cisplatin were divided into a control group and 54 patients treated with nimotuzumab combined with cisplatin were divided into an observation group. The two groups of patients were compared in terms of efficacy after treatment and incidence of adverse reactions. Changes of serum VEGF and MMP-2 concentrations before and after treatment were detected using enzyme-linked immunosorbent assay (ELISA), and the 3-year overall survival (OS) of patients was observed. RESULTS: Compared with the control group, patients in the observation group had significantly higher total remission rate (RR) (P < 0.05) and significantly lower incidence of adverse reactions (P < 0.05). Before treatment, there was no significant difference between the observation and control groups in the concentrations of VEGF and MMP-2 (P > 0.05). After treatment, the concentrations in the two groups were significantly lower than those before treatment (P < 0.05), and the concentrations in the observation group were significantly lower than those in the control group (P < 0.05). There was no significant difference in the 3-year OS between the observation and control groups (P > 0.05). CONCLUSIONS: Nimotuzumab combined with cisplatin could improve the conditions of patients with nasopharyngeal carcinoma. After treatment, the expression of VEGF and MMP-2 decreased significantly. We speculated that it improves the survival rate of patients by reducing the expression of VEGF and MMP-2.
Assuntos
Anticorpos Monoclonais Humanizados/administração & dosagem , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Cisplatino/administração & dosagem , Metaloproteinase 2 da Matriz/efeitos dos fármacos , Carcinoma Nasofaríngeo/tratamento farmacológico , Neoplasias Nasofaríngeas/tratamento farmacológico , Fator A de Crescimento do Endotélio Vascular/efeitos dos fármacos , Adulto , Anticorpos Monoclonais Humanizados/farmacologia , Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia , Cisplatino/farmacologia , Feminino , Humanos , Masculino , Pessoa de Meia-IdadeRESUMO
PURPOSE: P21-activated kinase 1 (PAK1), a serine/threonine protein kinase which functions downstream of RAC and CDC42 GTPase, is activated by a variety of stimuli, including RAS and other growth signaling factors. The extracellular signal kinase (ERK) and protein kinase B (AKT) signal pathways have been implicated in the pathogenesis of cancers. Whether PAK1 is sensitive to KRAS mutation signals and plays a role through ERK and AKT signaling pathways in NSCLC needs to be studied. METHODS: The expression of PAK1, ERK and AKT was detected in both lung cancer cell lines and clinical samples. PAK1 RNA interference and specific inhibitor of PAK1(IPA-3) were applied to lung cancer cell lines and mouse xenograft tumors. Cell growth was measured by MTT and colony formation assays. Cell migration and invasion were detected by wound healing and transwell assays. RAS mutation was detected by Taqman probe method. Correlation between KRAS, PAK1, ERK and AKT activities was analyzed in lung cancer patients. RESULTS: PAK1 was highly expressed not only in RAS mutant but also in RAS wild-type lung cancer cells. Using specific inhibitor of PAK1, IPA-3 and PAK1 RNA interference, cell proliferation, migration and invasion of lung cancer cells were reduced significantly, accompanied by decreased activities of ERK and AKT. Dual inhibition of ERK and AKT suppressed these cellular processes to levels comparable to those achieved by reduction in PAK1 expression. In NSCLC patients, PAK1 was not correlated with KRAS mutation but was significantly positively correlated with pERK and pAKT. CONCLUSION: PAK1 played roles in NSCLC proliferation and invasion via ERK and AKT signaling and suggested a therapeutic target for NSCLC.
Assuntos
Carcinoma Pulmonar de Células não Pequenas/metabolismo , Neoplasias Pulmonares/metabolismo , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores , Quinases Ativadas por p21/antagonistas & inibidores , Animais , Apoptose , Carcinoma Pulmonar de Células não Pequenas/enzimologia , Carcinoma Pulmonar de Células não Pequenas/patologia , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células/efeitos dos fármacos , Proliferação de Células/genética , Dissulfetos/farmacologia , Ativação Enzimática , Feminino , Genes ras/genética , Xenoenxertos , Humanos , Neoplasias Pulmonares/enzimologia , Neoplasias Pulmonares/patologia , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , Mutação , Naftóis/farmacologia , Invasividade Neoplásica , Proteínas Proto-Oncogênicas c-akt/metabolismo , Ensaio Tumoral de Célula-Tronco , CicatrizaçãoRESUMO
PURPOSE: To explore the regulatory relationship between Chloride intracellular channel 1 (CLIC1) and Angiomotin (AMOT)-p130, and reveal the role of AMOT-p130 in gastric cancer (GC). METHODS: Immunohistochemistry was performed to analyze the expression of CLIC1 and AMOT-p130 in GC tissues and adjacent tissues. The expression of AMOT-p130 upon CLIC1 silencing was analyzed using RT-PCR, western blot, and immunofluorescence in GC cells. Transwell and wound-healing assays were performed to detect migration and invasion in GC cells. The changes in EMT-related proteins were detected using western blot. RESULTS: Our study found that high CLIC1 expression was significantly associated with low AMOT-p130 expression in GC tissues. Silencing CLIC1 expression in MGC-803 cells (MGC-803 CLIC1 KO) and AGS cells (AGS CLIC1 KO) decreased the invasive and migratory abilities of tumor cells, which were induced by the upregulation of AMOT-p130. Subsequently, we demonstrated that AMOT-p130 inhibits the invasive and migratory abilities of GC cells by inhibiting epithelial-mesenchymal transition. CONCLUSIONS: Our study suggests that AMOT-p130 could inhibit epithelial-mesenchymal transition in GC cells. CLIC1 may participate in the metastatic progression of GC by downregulating the expression of AMOT-p130.
Assuntos
Canais de Cloreto/metabolismo , Transição Epitelial-Mesenquimal , Peptídeos e Proteínas de Sinalização Intercelular/metabolismo , Proteínas dos Microfilamentos/metabolismo , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patologia , Angiomotinas , Linhagem Celular Tumoral , Movimento Celular , Canais de Cloreto/genética , Feminino , Inativação Gênica , Humanos , Masculino , Pessoa de Meia-Idade , Invasividade Neoplásica , Proteínas de Neoplasias/genética , Proteínas de Neoplasias/metabolismo , Estadiamento de Neoplasias , Interferência de RNA , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Regulação para Cima , CicatrizaçãoRESUMO
PURPOSE: This study aimed to down-regulate LINC00667 and inhibit apoptosis and fibrosis of renal tubular epithelial cells through miR-34c. METHODS: Altogether, 98 patients with chronic kidney disease treated in our hospital were selected as the study group, and 67 normal people were selected as the control group. Epithelial cells of proximal convoluted tubules in human renal cortex were purchased. TGF-ß1 was used to induce fibrosis of HK-2 renal tubular epithelial cells. The expression of LINC00667, miR-34c, type I collagen (Col 1) and type III collagen (Col 3) were detected by qRT-PCR and WB. RESULTS: LINC00667 was highly expressed in cancer tissues and HK-2, while miR-34c was poorly expressed. Inhibition of LINC00667 and over-expression of miR-34c could inhibit the proliferation and invasion of chronic kidney disease cells, but increase the apoptosis rate. Down-regulation of LINC00667 could significantly reduce of Col 1 and Col 3 in renal interstitial fibroblasts induced by TGF-ß1, while up-regulation of miR-34c could also achieve this effect. Double luciferase report confirmed that there was a targeted regulatory relationship between LINC00667 and miR-34c. CONCLUSION: LINC00667 could reduce the proliferation and invasion of chronic kidney disease cells, increase the apoptosis rate by regulating miR-34c, and improve renal fibrosis.
Assuntos
Células Epiteliais/fisiologia , Túbulos Renais Proximais/metabolismo , MicroRNAs/metabolismo , RNA Longo não Codificante/metabolismo , Insuficiência Renal Crônica/metabolismo , Apoptose , Estudos de Casos e Controles , Proliferação de Células , Colágeno Tipo I/metabolismo , Colágeno Tipo III/metabolismo , Regulação para Baixo , Células Epiteliais/patologia , Fibroblastos/metabolismo , Fibrose , Humanos , Túbulos Renais Proximais/patologia , Invasividade Neoplásica , Insuficiência Renal Crônica/patologia , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Fator de Crescimento Transformador beta1RESUMO
OBJECTIVE: To investigate the polarization of human acute monocytic leukemia THP-1 cells-derived macrophages induced by Nippostrongylus brasiliensis proteins in vitro, so as to provide insights into the elucidation of the mechanisms underlying host immune responses to hookworm infections. METHODS: The in-vitro culture of N. brasiliensis was established and maintained in the laboratory, and the third- (L3) and fifth-stage larvae (L5) were collected under a sterile condition for preparation of L3 and L5 proteins. The in-vitro culture of THP-1 cells was established, stimulated with 500 ng/mL PMA to yield M0 macrophages that were adherent to the plate wall. The LPS + IFN-γ group, IL-4 + IL-13 group, L3 protein group and L5 protein group were given stimulation with 500 ng/mL LPS plus 100 ng/mL IFN-γ, IL-4 and IL-13 (both 100 ng/mL), L3 protein (5 mg/mL) and L5 protein (5 mg/mL), respectively, while the negative control group was given no stimulation. The cell morphology was observed using microscopy, the mRNA expression of M1/M2 macrophages-specific genes was quantified using a quantitative real-time PCR (qPCR) assay, and the surface markers of M1/M2 macrophages were detected using flow cytometry, while the levels of cytokines secreted by M1/M2 macrophages were measured using enzyme-linked immunosorbent assay (ELISA) following stimulations, so as to examine the polarization of THP-1-derived macrophages induced by N. brasiliensis proteins in vitro. RESULTS: Following stimulation with PMA, THP-1 cells appeared wall-adherent M0 macrophages, and polarized to typical M1 macrophages following stimulation with LPS + IFN-γ, and typical M2 macrophages following stimulation with IL-4 + IL-13, IL-3 protein or L5 protein. There was a significant difference in the proportion of M1 macrophages among the negative control group, the LPS + IFN-γ group, the IL-4 + IL-13 group, the L3 protein group and the L5 protein group (χ2 = 3 721.00, P < 0.001), with the highest proportion detected in the LPS + IFN-γ group, and there was also a significant difference in the proportion of M2 macrophages among groups (χ2 = 105.43, P < 0.001). There were significant differences among groups in terms of the mRNA expression of CCL2 (F = 191.95, P < 0.001), TNF-α (F = 129.95, P < 0.001), IL-12b (F = 82.89, P < 0.001), PPARγ (F = 11.30, P < 0.001), IL-10 (F = 9.51, P < 0.001) and Mrc1 genes (F = 12.35, P < 0.001). In addition, there were significant differences in the proportion of positive CD86 and CD206 expression among groups (χ2 = 24 004.33 and 832.50, P < 0.001). Higher IL-1ß and TNF-α levels were measured in the LPS + IFN-γ group than in the IL-4 + IL-13 group, the L3 protein group and the L5 protein group (P < 0.001), and greater TGF-ß1 and IL-10 levels were seen in the IL-4 + IL-13 group, the L3 protein group and the L5 protein group than in the negative control group and the LPS + IFN-γ group (P < 0.05). CONCLUSIONS: Both L3 and L5 proteins of N. brasiliensis may induce the polarization of THP-1-derived macrophages to M2 type in vitro.
Assuntos
Leucemia Monocítica Aguda , Animais , Antígenos de Helmintos/farmacologia , Criança , Humanos , Lipopolissacarídeos , Macrófagos/efeitos dos fármacos , Nippostrongylus/química , Células THP-1/citologia , Células THP-1/efeitos dos fármacosRESUMO
BACKGROUND: The incidence of breast cancer (BC) is the highest among women. Identification of miRNAs as biomarkers may help to improve the diagnosis of BC. The purpose of this study was to assess the expression levels of miR-1976 in plasma samples and the biological functions in the progression of BC. METHODS: The expression levels of miR-1976 in plasma samples and tissues were measured by quantitative real-time polymerase chain reaction (qRT-PCR). The associations between the expression levels and clinicopathological features were studied. Cell supernatants were used to simulate circulation. The biological functions of miR-1976 were assessed in vitro and in vivo. RESULTS: The expression levels of miR-1976 in plasma samples were found significantly lower in patients with BC than those in healthy controls, and were associated with Ki-67. The expression levels in BC tissues were lower than those in adjacent normal tissues, and were correlated with the number of lymph nodes and Ki-67. The expression levels in BC cell supernatants and cell lines were lower than that in normal human breast epithelial cell line HBL-100. miR-1976 knockdown promoted proliferation in vitro and in vivo. CONCLUSION: miR-1976 may serve as a promising non-invasive biomarker for the diagnosis of BC in the future.
Assuntos
Neoplasias da Mama/etiologia , MicroRNAs/fisiologia , Animais , Neoplasias da Mama/genética , Neoplasias da Mama/patologia , Linhagem Celular Tumoral , Proliferação de Células , Progressão da Doença , Exossomos , Feminino , Humanos , Camundongos , Camundongos Endogâmicos BALB C , MicroRNAs/sangueRESUMO
BACKGROUND: Biofilm formation has been shown to be associated with damaged areas of endoscope channels. It was hypothesized that the passage of instruments and brushes through endoscope channels during procedures and cleaning contributes to channel damage, bacterial attachment and biofilm formation. AIM: To compare surface roughness and bacterial attachment in used and new endoscope channels in vivo and in vitro. METHODS: Surface roughness of 10 clinically used (retired) and seven new colonoscope biopsy channels was analysed by a surface profiler. For the in-vitro study, a flexible endoscope biopsy forceps was passed repeatedly through a curved 3.0-mm-diameter Teflon tube 100, 200 and 500 times. Atomic force microscopy was used to determine the degree of inner surface damage. The number of Escherichia coli or Enterococcus faecium attached to the inner surface of the new Teflon tube and the tube with 500 forceps passes in 1 h at 37oC was determined by culture. RESULTS: The average surface roughness of the used biopsy channels was found to be 1.5 times greater than that of the new biopsy channels (P=0.03). Surface roughness of Teflon tubes with 100, 200 and 500 forceps passes was 1.05-, 1.12- and 3.2-fold (P=0.025) greater than the roughness of the new Teflon tubes, respectively. The number of E. coli and E. faecium attached to Teflon tubes with 500 forceps passes was 2.9-fold (P=0.021) and 4.3-fold (P=0.004) higher compared with the number of E. coli and E. faecium attached to the new Teflon tubes, respectively. CONCLUSION: An association was found between endoscope usage with damage to the biopsy channel and increased bacterial attachment.
Assuntos
Aderência Bacteriana , Endoscópios/microbiologia , Enterococcus faecium/fisiologia , Contaminação de Equipamentos/prevenção & controle , Escherichia coli/fisiologia , Biofilmes/crescimento & desenvolvimento , Desinfecção/métodos , Politetrafluoretileno , Propriedades de SuperfícieRESUMO
BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is a kind of cancer with heterogeneous biological characteristics, which is affected by a complex network of gene interactions. Identification of molecular biomarkers paves the way for individualized therapy based on gene expression profiles, which can overcome the heterogeneity of ESCC. METHODS: In this study, GSE20347, GSE23400 and GSE45670 datasets were retrieved from Gene Expression Omnibus (GEO) database, and the overlapping differentially expressed genes (DEGs) in three datasets were screened. Then the overlapping DEGs function was annotated by Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway-enrichment analysis. The prognostic value of the top five KEGG pathway-related genes were further validated in The Cancer Genome Atlas (TCGA) database. After extensive statistical analysis, four genes (CDC25B, CXCL8, FZD6 and MCM4) were identified as potential prognostic markers. Among the four candidate genes, the prognostic value of FZD6 in ESCC patients has not been evaluated. Therefore, we finally used immunohistochemistry method to evaluate the effect of FZD6 on the prognosis of patients with ESCC. Additionally, we detected the expression level of FZD6 in ESCC cell line and normal esophageal epithelial cell line, and observed the cell viability of ESCC cell line after FZD6 knockdown. RESULTS: The results showed that the overexpression of FZD6 predicted poor overall survival (OS) (P = 0.005) and progression-free survival (PFS) (P = 0.004) in ESCC patients. COX regression analysis showed that N stage (P = 0.026) and FZD6 expression level (P = 0.001) were independent prognostic factors of OS for ESCC patients. Furthermore, compared with normal esophageal epithelial cell line, the up-regulation of FZD6 was detected in ESCC cell line. Knockdown of FZD6 could significantly inhibit the proliferation of ESCC cells (P < 0.001). CONCLUSION: CDC25B, CXCL8, FZD6 and MCM4 were screened as candidate genes for prognosis assessment of patients with ESCC. The prognostic role of FZD6 in ESCC patients was confirmed in current study.
Assuntos
Neoplasias Esofágicas/genética , Carcinoma de Células Escamosas do Esôfago/genética , Receptores Frizzled/genética , Linhagem Celular Tumoral , Sobrevivência Celular/genética , Feminino , Técnicas de Silenciamento de Genes , Humanos , Imuno-Histoquímica , Técnicas In Vitro , Interleucina-8/genética , Masculino , Pessoa de Meia-Idade , Componente 4 do Complexo de Manutenção de Minicromossomo/genética , Intervalo Livre de Progressão , Modelos de Riscos Proporcionais , RNA Interferente Pequeno , Taxa de Sobrevida , Regulação para Cima , Fosfatases cdc25/genéticaRESUMO
PURPOSE: Vitexin, an inhibitor of hypoxia-inducible factor (HIF)-1α, has anti-tumor effect. However, whether it can enhance the radiotherapy sensitization of hyperbaric oxygen (HBO) on glioma is unclear. This study aimed to investigate the effect of vitexin. METHODS: The nude mice with paw-transplanted glioma were divided into four groups: control group, HBO + radiation group, HBO + vitexin group, and HBO + vitexin + radiation group. The mice of last two groups were daily given vitexin 75 mg/kg by intraperitoneal injection. 30 min after administration of vitexin, the HBO-treated mice were daily placed in HBO chamber for 60 min. The radiation-treated mice were given local tumor irradiation once every week during the HBO treatment, and the dose of irradiation was 10 Gy/time. The experimental treatment lasted for 21 days. RESULTS: Compared with the HBO + radiation group, the tumor volume, tumor weight, and tumor weight coefficient in the HBO + vitexin + radiation group were lower (p < 0.05). Importantly, the contents of reduced glutathione and glutathione peroxidase as well as expressions of HIF-1α, vascular endothelial growth factor, glucose transporter (GLUT)-1, and GLUT-3 proteins in tumor tissues were also lower in the HBO + vitexin + radiation group than in the HBO + radiation group (p < 0.01). CONCLUSIONS: Vitexin can cooperate with HBO to sensitize the glioma radiotherapy, and its mechanisms may be correlated to the inhibition of HIF-1α protein expression and subsequent decrements of its downstream protein expressions, which finally cause the reduction of antioxidant capacity.
Assuntos
Apigenina/farmacologia , Glioma/radioterapia , Oxigenoterapia Hiperbárica , Tolerância a Radiação/efeitos dos fármacos , Carga Tumoral/efeitos dos fármacos , Carga Tumoral/efeitos da radiação , Animais , Linhagem Celular Tumoral , Glioma/metabolismo , Glioma/patologia , Transportador de Glucose Tipo 1/efeitos dos fármacos , Transportador de Glucose Tipo 1/metabolismo , Transportador de Glucose Tipo 3/efeitos dos fármacos , Transportador de Glucose Tipo 3/metabolismo , Glutationa/efeitos dos fármacos , Glutationa/metabolismo , Glutationa Peroxidase/efeitos dos fármacos , Glutationa Peroxidase/metabolismo , Humanos , Subunidade alfa do Fator 1 Induzível por Hipóxia/antagonistas & inibidores , Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo , Camundongos , Camundongos Nus , Transplante de Neoplasias , Fator A de Crescimento do Endotélio Vascular/efeitos dos fármacos , Fator A de Crescimento do Endotélio Vascular/metabolismoRESUMO
Over-accumulation of triglycerides (TGs) in goose hepatocytes leads to the formation of fatty acid liver. Phosphoenolpyruvate carboxylase kinase 1 (PEPCK) is regarded as the rate-limiting enzyme for gluconeogenesis, and there is evidence that PEPCK is involved in regulating hepatic glucolipid metabolism. Hence, we proposed that PEPCK may have a role in goose hepatic steatosis. To test our hypothesis, the present study was conducted to firstly determine the sequence characteristics of goose PEPCK and then to explore its role in overfeeding-induced fatty liver. Our results showed that goose PEPCK encodes a 622-amino-acids protein that contains highly conserved oxaloacetate-binding domain, kinase-1 and kinase-2 motifs. PEPCK had higher mRNA levels in goose liver, and overfeeding markedly increased its expression in livers of both Sichuan White and Landes geese (p 0.05). Besides, expression of PEPCK was positively correlated with hepatic TG levels as well as plasma glucose and insulin concentrations. Additionally, in cultured goose primary hepatocyte, treatment with either oleic acid (0.8, 1.2 or 1.6 mM) or linoleic acid (0.125 or 0.25 mM) significantly (p 0.05) enhanced the expression of PEPCK. Taken together, these data suggested a role for PEPCK in the occurrence of overfeeding-induced goose hepatic steatosis.(AU)
Assuntos
Animais , Gansos/metabolismo , Gansos/fisiologia , Fosfoenolpiruvato Carboxilase/análise , Fosfoenolpiruvato Carboxilase/química , Fosfoenolpiruvato Carboxilase/genética , Fígado Gorduroso , HiperfagiaRESUMO
This experiment aimed to investigate whether Escherichia coli (E. coli) infection could affect the TGF-/smads signaling pathway in the jejunal tissue of chickens. One-day-old Cobb 500 broilers were randomly divided into 2 groups and treated with intraperitoneal E. coli or broth injection. Clinical signs of the birds were assessed every day. Spleen and bursa of Fabricius of the birds, post-infection (pi), were collected to evaluate immune organ index. Jejunal tissues were collected to ascertain the expression of TGF-s, TRs, and Smads. The results showed that the infected birds had significantly higher index of the spleen (24hrs and 48hrs pi) compared with birds in the control group (p 0.05). The relative gene expression of TGF-4 increased (p 0.05), while the expression of Smad7 down-regulated in the E. coli group (p 0.01). There was no significant difference in TGF-2, TGF-3, TR I, TR II, Smad2, Smad3 expression (p>0.05). In conclusion, TGF-/Smad signaling pathway was associated with the immune response of broilers in E. coli infection and TGF-4 was the main subtype interacting with E. coli infection.(AU)
Assuntos
Animais , Galinhas/genética , Galinhas/microbiologia , Galinhas/fisiologia , Fator de Crescimento Transformador beta/análise , Fator de Crescimento Transformador beta/genética , Intestinos/lesõesRESUMO
Over-accumulation of triglycerides (TGs) in goose hepatocytes leads to the formation of fatty acid liver. Phosphoenolpyruvate carboxylase kinase 1 (PEPCK) is regarded as the rate-limiting enzyme for gluconeogenesis, and there is evidence that PEPCK is involved in regulating hepatic glucolipid metabolism. Hence, we proposed that PEPCK may have a role in goose hepatic steatosis. To test our hypothesis, the present study was conducted to firstly determine the sequence characteristics of goose PEPCK and then to explore its role in overfeeding-induced fatty liver. Our results showed that goose PEPCK encodes a 622-amino-acids protein that contains highly conserved oxaloacetate-binding domain, kinase-1 and kinase-2 motifs. PEPCK had higher mRNA levels in goose liver, and overfeeding markedly increased its expression in livers of both Sichuan White and Landes geese (p 0.05). Besides, expression of PEPCK was positively correlated with hepatic TG levels as well as plasma glucose and insulin concentrations. Additionally, in cultured goose primary hepatocyte, treatment with either oleic acid (0.8, 1.2 or 1.6 mM) or linoleic acid (0.125 or 0.25 mM) significantly (p 0.05) enhanced the expression of PEPCK. Taken together, these data suggested a role for PEPCK in the occurrence of overfeeding-induced goose hepatic steatosis.