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OBJECTIVE: Gastric cancer (GC) is one of the malignant tumors with the highest mortality worldwide. Our previous studies have revealed that LINC00691 is up-regulated in serum of GC patients as a novel potential biomarker for GC diagnosis and prognosis. However, the roles of serum exosomal LINC00691 in GC has not been clarified. This study aimed to find the expression pattern of serum exosomal LINC00691 in GC patients and the correlation between the level of serum exosomal LINC00691 and the pathology of gastric cancer patients. METHODS: We collected the serum of 94 GC patients before surgery and extracted exosomes to detect the expression level of exosomal LINC00691, with 21 healthy volunteers and 17 patients with benign gastric diseases as controls. Surgical GC tissues and paired healthy tissues were collected to culture primary cancer-associated fibroblasts (CAFs) and normal fibroblasts (NFs). We then treated NFs with LINC00691-rich GC cell culture supernatant or exosomes and detected the activation markers and biological functions of the fibroblasts. RESULTS: The results of real-time qPCR indicated that the serum exosomal LINC00691 of GC patients was significantly higher than that of healthy subjects and patients with benign gastric diseases, and was associated with the clinicopathology of GC patients. More interestingly, when the NFs were treated with GC exosomes, the level of LINC00691 was significantly increased, the cell proliferation and migration were noticeably enhanced, and the ability to accelerate GC cell proliferation and invasion was promoted, which means that the induced fibroblasts gained the properties of CAFs. In addition, we found that knockdown of LINC00691 and the use of the JAK2/STAT3 signaling pathway inhibitor ruxolitinib effectively deprived exosome-containing GC cell supernatants of the effects on NFs. CONCLUSION: Our study suggested that exosomal LINC00691 promoted NFs to gained the properties of CAFs depending on JAK2/STAT3 signaling pathway as a potential diagnostic biomarker for GC.
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Fibroblastos Asociados al Cáncer , Exosomas , MicroARNs , Neoplasias Gástricas , Humanos , Fibroblastos Asociados al Cáncer/metabolismo , MicroARNs/metabolismo , Neoplasias Gástricas/genética , Neoplasias Gástricas/cirugía , Neoplasias Gástricas/metabolismo , Exosomas/genética , Exosomas/metabolismo , Línea Celular Tumoral , Proliferación Celular/genética , Movimiento Celular/genéticaRESUMEN
Tumor immunity is a growing field of research that involves immune cells within the tumor microenvironment. Neutrophil extracellular traps (NETs) are neutrophil-derived extracellular web-like chromatin structures that are composed of histones and granule proteins. Initially discovered as the predominant host defense against pathogens, NETs have attracted increasing attention due to they have also been tightly associated with tumor. Excessive NET formation has been linked to increased tumor growth, metastasis, and drug resistance. Moreover, through direct and/or indirect effects on immune cells, an abnormal increase in NETs benefits immune exclusion and inhibits T-cell mediated antitumor immune responses. In this review, we summarize the recent but rapid progress in understanding the pivotal roles of NETs in tumor and anti-tumor immunity, highlighting the most relevant challenges in the field. We believe that NETs may be a promising therapeutic target for tumor immunotherapy.
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Trampas Extracelulares , Neoplasias , Humanos , Neutrófilos , Cromatina/metabolismo , Histonas/metabolismo , Neoplasias/metabolismo , Inmunoterapia , Microambiente TumoralRESUMEN
Antinuclear antibodies (ANAs) are a spectrum of autoantibodies that react with cell nucleus structures. ANA assay is a screening test for the diagnosis of autoimmune disease. Although many patients with positive ANA did not develop autoimmune diseases, it is unclear whether high concentrations of ANA have potential damage to the body. In this study, we conducted an epidemiological survey of ANAs in healthy population, and further examined the associations of ANA with clinical laboratory indicators, inflammation indicators and immune function indicators in a large health checkup population-based cohort. We found the positive rate of ANA was 7.09%, of which the positive rate of female (10.2%) was higher than that of male (4.6%). Moreover, our data showed that ANA positive population present a higher rate of metabolic abnormalities than control group. We further detected the inflammatory and immune-related indicators of ANA positive population, and found that high ANA was correlated with inflammatory and immune dysfunction. In conclusion, our results indicated that the positive rate of ANA was high in healthy population. Moreover, high levels of ANAmight be involved in the metabolic abnormalities, inflammation and immune dysfunction. Thus, ANA testing should be routine for healthy people, and to avoid misdiagnosis, those who had clinical symptoms should be further examined for the subtype of ANA present in the serum.
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Anticuerpos Antinucleares , Enfermedades Autoinmunes , Humanos , Masculino , Femenino , Autoanticuerpos , Enfermedades Autoinmunes/diagnóstico , Enfermedades Autoinmunes/epidemiología , Estudios de Cohortes , InflamaciónRESUMEN
Dynamic changes in metabolites may affect liver disease progression, and provide new methods for predicting liver damage. We used ultra-performance liquid chromatography-mass spectroscopy to assess serum metabolites in healthy controls (HC), and patients with acute hepatitis E (AHE) or hepatitis E virus acute liver failure (HEV-ALF). The principal component analysis, partial least squares discriminant analysis, and discriminant analysis of orthogonal projections to latent structures models illustrated significant differences in the metabolite components between AHE patients and HCs, or between HEV-ALF and AHE patients. In pathway enrichment analysis, we further identified two altered pathways, including linoleic acid metabolism and phenylalanine, tyrosine, and tryptophan biosynthesis, when comparing AHE patients with HCs. Linoleic acid metabolism and porphyrin and chlorophyll metabolism pathways were significantly different in HEV-ALF when compared with AHE patients. The discriminative performances of differential metabolites showed that taurocholic acid, glycocholic acid, glycochenodeoxycholate-3-sulfate, and docosahexaenoic acid could be used to distinguish HEV-ALF from AHE patients. The serum levels of glycocholic acid, taurocholic acid, deoxycholic acid glycine conjugate, and docosahexaenoic acid were associated with the prognosis of HEV-ALF patients. Dynamic changes in serum metabolites were associated with AHE infection and severity. The identified metabolites can be used to diagnose and predict the prognosis of HEV-ALF.
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Virus de la Hepatitis E , Hepatitis E , Enfermedad Aguda , Ácidos Docosahexaenoicos , Ácido Glicocólico , Humanos , Ácido Linoleico , Ácido TaurocólicoRESUMEN
Epidermal growth factor receptor (EGFR) signalling and the interleukin-6 (IL-6)/signal transducer and activator of transcription 3 (STAT3) are aberrantly activated in ovarian cancer. However, inhibition of EGFR signalling in ovarian cancer patients resulted in a disappointing clinical benefit. In this study, we found that EGFR could activate IL-6-STAT3 pathway in ovarian cancer cells. However, we also demonstrated that EGFR knockdown could increase STAT3 phosphorylation in HO8910 and OVCAR-3 ovarian cancer cells. Interestingly, we further demonstrated that the non-coding RNA miR-146b could simultaneously block both the EGFR and IL-6-STAT3 pathways. Finally, our data demonstrated that miR-146b overexpression resulted in a greater suppression of cell migration than STAT3 pathway inhibition alone.These results suggest a complex and heterogeneous role of EGFR in ovarian cancer. Combined blockade of EGFR and IL-6-STAT3 pathways by miR-146b might be a strategy for improving the clinical benefit of targeting the EGFR pathway in ovarian cancer patients in the future.
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Carcinoma Epitelial de Ovario/metabolismo , Receptores ErbB/metabolismo , Interleucina-6/metabolismo , MicroARNs/metabolismo , Neoplasias Ováricas/metabolismo , Factor de Transcripción STAT3/metabolismo , Línea Celular Tumoral , Movimiento Celular , Proliferación Celular , Receptores ErbB/genética , Femenino , Regulación de la Expresión Génica , Técnicas de Silenciamiento del Gen , Humanos , Fosforilación , Transducción de SeñalRESUMEN
Long noncoding RNAs (lncRNAs) have been reported to be associated with the progression of coronary artery disease (CAD). In our previous study, the levels of lncRNA uc003pxg.1 were upregulated in patients with CAD compared with those in control subjects. However, the role and underlying mechanism of the effects of uc003pxg.1 in CAD remain unknown. Therefore, the aim of the present study was to investigate the expression pattern and biological function of uc003pxg.1 in CAD. First, uc003pxg.1 expression levels were assessed in peripheral blood mononuclear cells isolated from patients with CAD by reverse transcriptionquantitative (RTq)PCR. The results demonstrated that the levels of uc003pxg.1 were significantly upregulated (~4.6fold) in samples from 80 patients with CAD compared with those in 80 healthy subjects. Subsequently, the present study demonstrated that small interfering RNAmediated uc003pxg.1 knockdown inhibited human umbilical vein endothelial cell (HUVEC) proliferation and migration, which was analyzed using the Cell Counting Kit8, cell cycle, EdU and Transwell assays. Additionally, the results of RTqPCR and western blot analyses revealed that uc003pxg.1 regulated the mRNA and protein levels of cyclin D1 and cyclindependent kinase. Through highthroughput sequencing and dualluciferase reporter assays, the present study demonstrated that microRNA (miR)255p was a downstream target of uc003pxg.1. Further experiments verified that uc003pxg.1 regulated HUVEC proliferation and migration via miR255p. The results of the present study may enhance the current understanding of the role of lncRNA uc003pxg.1 in CAD.
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Movimiento Celular/genética , Proliferación Celular/genética , Enfermedad de la Arteria Coronaria/genética , Células Endoteliales de la Vena Umbilical Humana/metabolismo , MicroARNs/genética , ARN Largo no Codificante/genética , Adulto , Anciano , Anciano de 80 o más Años , Secuencia de Bases , Ciclo Celular/genética , Proteínas de Ciclo Celular/genética , Proteínas de Ciclo Celular/metabolismo , Células Cultivadas , Enfermedad de la Arteria Coronaria/metabolismo , Enfermedad de la Arteria Coronaria/patología , Femenino , Perfilación de la Expresión Génica/métodos , Humanos , Masculino , Persona de Mediana Edad , RNA-Seq/métodos , Homología de Secuencia de Ácido NucleicoRESUMEN
BACKGROUND: The genomic copy number of LINC01061 is amplified in papillary thyroid cancer. However, its role in gastric cancer is not clear. MATERIALS AND METHODS: Tissues and serum of GC patients were collected to detect the expression of LINC01061 by quantitative real-time polymerase chain reaction (qRT-PCR). ShRNA were applied to knock down the expression of LINC01061. Growth curves and colony formation experiments were applied to evaluate cell growth. Cell migration was assessed by transwell migration experiments. Cell cycle and apoptosis were analyzed by flow cytometry. Epithelial-mesenchymal transition (EMT) was examined by qRT-PCR and Western blot. RESULTS: The expression of LINC01061 was upregulated in tissues and serum of GC patients and it was associated with the clinicopathological features and survival time. Functional study indicated that cell growth and migration were suppressed after LINC01061 knockdown. Cell cycle arrest and increased apoptosis occurred when LINC01061 expression was inhibited. EMT was also impaired combined with a decrease in ß-catenin expression after LINC01061 knockdown. CONCLUSIONS: Our data indicate that LINC01061 is a novel biomarker for diagnosis and prognosis of GC. LINC01061 promoted progression of GC through cell cycle regulation and EMT.
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Neoplasias Gástricas , Neoplasias de la Tiroides , Biomarcadores , Línea Celular Tumoral , Movimiento Celular , Proliferación Celular , Transición Epitelial-Mesenquimal , Regulación Neoplásica de la Expresión Génica , Humanos , Invasividad Neoplásica , ARN Largo no Codificante , Neoplasias Gástricas/genética , Neoplasias de la Tiroides/genéticaRESUMEN
Epithelial ovarian carcinoma (EOC) is the most lethal gynecologic malignancy. However, the molecular mechanisms remain unclear. In this study, we found that miR-146b was downregulated in EOC and its expression level was negatively correlated with the pathological staging. Follow-up functional experiments illustrated that overexpression of miR-146b significantly inhibited cell migration and invasion, and increased cell proliferation, but it also improved the response to chemotherapeutic agents. Mechanistically, we demonstrated that miR-146b exerted its function mainly through inhibiting F-box and leucine-rich repeat protein 10 (FBXL10), and upregulated the Cyclin D1, vimentin (VIM), and zona-occludens-1 (ZO-1) expression in EOC. These findings indicate that miR-146b-FBXL10 axis is an important epigenetic regulation pathway in EOC. Low miR-146b may contribute to cancer progression from primary stage to advanced stage, and may be the promising therapeutic target of EOC.
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Carcinoma Epitelial de Ovario/genética , Resistencia a Antineoplásicos/genética , Proteínas F-Box/genética , Regulación Neoplásica de la Expresión Génica , Histona Demetilasas con Dominio de Jumonji/genética , MicroARNs/genética , Neoplasias Ováricas/genética , Adulto , Animales , Antineoplásicos/farmacología , Carcinoma Epitelial de Ovario/tratamiento farmacológico , Carcinoma Epitelial de Ovario/metabolismo , Carcinoma Epitelial de Ovario/patología , Línea Celular Tumoral , Movimiento Celular/efectos de los fármacos , Proliferación Celular/efectos de los fármacos , Cisplatino/farmacología , Ciclina D1/genética , Ciclina D1/metabolismo , Resistencia a Antineoplásicos/efectos de los fármacos , Epigénesis Genética , Proteínas F-Box/antagonistas & inhibidores , Proteínas F-Box/metabolismo , Femenino , Humanos , Histona Demetilasas con Dominio de Jumonji/antagonistas & inhibidores , Histona Demetilasas con Dominio de Jumonji/metabolismo , Ratones , Ratones Desnudos , MicroARNs/metabolismo , Persona de Mediana Edad , Estadificación de Neoplasias , Neoplasias Ováricas/tratamiento farmacológico , Neoplasias Ováricas/metabolismo , Neoplasias Ováricas/patología , Paclitaxel/farmacología , ARN Interferente Pequeño/genética , ARN Interferente Pequeño/metabolismo , Transducción de Señal , Carga Tumoral/efectos de los fármacos , Vimentina/genética , Vimentina/metabolismo , Ensayos Antitumor por Modelo de Xenoinjerto , Proteína de la Zonula Occludens-1/genética , Proteína de la Zonula Occludens-1/metabolismoRESUMEN
Epithelial ovarian cancer (EOC) is the most lethal gynecological malignancy. LIN28 homolog A (LIN28A) is a RNAbinding protein, which serves a fundamental role in cell development and pluripotency. Pololike kinase 4 (PLK4) is a member of the pololike kinase family, which primarily takes part in the mitotic regulation. Overexpression of LIN28A has been demonstrated in ovarian cancer; however, the expression of PLK4 and the correlation between the expression of LIN28A and PLK4 in EOC has not been discussed. In the present study, the mRNA and protein levels of LIN28A and PLK4 were evaluated by reverse transcriptionquantitative polymerase chain reaction and immunohistochemistry in ovarian tissues of patients. Results demonstrated significantly increased expression in EOC compared with benign epithelial ovarian tumors. High expression of LIN28A and PLK4 was detected at the advanced pathological stage. Furthermore, PLK4 expression was positively correlated with LIN28A (r=0.555; P=0.039). The median survival analysis of patients with EOC with LIN28A and PLK4 double positive expression was 14 months, compared with 30 months in single positive and 60 months in double negative patients by KaplanMeier analysis (P<0.05). The expressions of LIN28A and PLK4 was elevated in different EOC cell lines compared to with a normal ovarian cell line. The 293T cells transfected with LIN28A plus a PLK4 plasmid were the fastestgrowing group. These results suggest that coexpression of LIN28A and PLK4 may be associated with poor prognosis of EOC and could serve as promising prognostic biomarkers and therapeutic targets in EOC. LIN28A and PLK4 may be used along with traditional morphological and clinical characteristics for predicting prognosis.
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Carcinoma Epitelial de Ovario/genética , Carcinoma Epitelial de Ovario/mortalidad , Regulación Neoplásica de la Expresión Génica , Proteínas Serina-Treonina Quinasas/genética , Proteínas de Unión al ARN/genética , Adulto , Anciano , Biomarcadores de Tumor , Carcinoma Epitelial de Ovario/patología , Línea Celular Tumoral , Femenino , Humanos , Inmunohistoquímica , Estimación de Kaplan-Meier , Persona de Mediana Edad , Clasificación del Tumor , Estadificación de Neoplasias , Oportunidad Relativa , Pronóstico , Proteínas Serina-Treonina Quinasas/metabolismo , Proteínas de Unión al ARN/metabolismo , Adulto JovenRESUMEN
The discovery of histone demethylases has revealed the dynamic nature of the regulation of histone methylation. KDM2B is an important histone lysine demethylase that removes methyl from H3K36me2 and H3K4me3. It participates in many aspects of normal cellular processes such as cell senescence, cell differentiation and stem cell self-renewal. Recent studies also showed that KDM2B was overexpressed in various types of cancers. This review focuses primarily on the current knowledge of KDM2B and its function in cancer development.
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Major depression disorder (MDD) has become increasingly common in patients with ovarian cancer, which complicates the treatment course. The microRNA (miRNA)-mRNA regulation network may help elucidate the potential mechanism of MDD in ovarian cancer. The differentially expressed microRNAs (DEmiRs) and mRNAs (DEmRNAs) were therefore identified from the GSE61741, GSE58105 and GSE9116 ovarian cancer datasets using GEO2R. The target genes of the DEmiRs were then obtained using the TargetScan, microRNAorg, microT-CDS, miRDB and miRTarBase prediction tools. The DAVID program was used to identify the KEGG pathways of target genes, and the core genes of major depressive disorder (MDD) were identified using the Kaplan-Meier Plotter for ovarian cancer. A total of 5 DEmiRs (miR-23b-3p, miR-33b-3p, miR-1265, miR-933 and miR-629-5p) were obtained from GSE61741 and GSE58105. The target genes of these DEmiRs were enriched in pathways that were considered high risk for developing MDD in ovarian cancer. A total of 11 risk genes were selected from these pathways as the core genes in the miRNA-mRNA network of MDD in ovarian cancer, and eventually identified the following 12 miRNA-mRNAs pairs: miR-629-5p-FGF1, miR-629-5p-AKT3, miR-629-5p-MAGI2, miR-933-BDNF, miR-933-MEF2A, miR-23b-3p-TJP1, miR-23b-3p-JMJD1, miR-23b-3p-APAF1, miR-23b-3p-CAB39, miR-1265-CDKN1B, miR-33b-3p-CDKN1B, and miR-33b-3p-F2R. These results may provide novel insights into the mechanisms of developing MDD in ovarian cancer patients.
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Increasing evidence has experimentally proved the competitive endogenous RNA (ceRNA) hypothesis that long non-coding RNA (lncRNA) can affect the expression of RNA targets by competitively combining microRNA (miRNA) via miRNA response elements. However, an extensive ceRNA network of thyroid carcinoma in a large cohort has not been evaluated. We analyzed the RNAseq and miRNAseq data of 348 cases of primary papillary thyroid cancer (PTC) patients with clinical information downloaded from The Cancer Genome Atlas (TCGA) project to search for potential biomarkers or therapeutic targets. A computational approach was applied to build an lncRNA-miRNA-mRNA regulatory network of PTC. In total, 780 lncRNAs were detected as collectively dysregulated lncRNAs in all 3 PTC variants compared with normal tissues (fold change >2 and false discovery rate <0.05). The interactions among 45 lncRNAs, 13 miRNAs and 86 mRNAs constituted a ceRNA network of PTC. Nine out of the 45 aberrantly expressed lncRNAs were related to the clinical features of PTC patients. However, the expression levels of 3 lncRNAs (LINC00284, RBMS3-AS1 and ZFX-AS1) were identified to be tightly correlated with the patients overall survival (log-rank, P<0.05). The present study identified a list of specific lncRNAs associated with PTC progression and prognosis. This complex ceRNA interaction network in PTC may provide guidance for better understanding the molecular mechanisms underlying PTC.
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Adenocarcinoma Folicular/genética , Biomarcadores de Tumor/genética , Carcinoma Papilar/genética , Regulación Neoplásica de la Expresión Génica , Redes Reguladoras de Genes , ARN Largo no Codificante/genética , Neoplasias de la Tiroides/genética , Adenocarcinoma Folicular/patología , Carcinoma Papilar/patología , Estudios de Casos y Controles , Estudios de Cohortes , Bases de Datos Genéticas , Femenino , Estudios de Seguimiento , Humanos , Masculino , MicroARNs , Persona de Mediana Edad , Pronóstico , ARN Mensajero , Tasa de Supervivencia , Neoplasias de la Tiroides/patologíaRESUMEN
DNA microarray and high-throughput sequencing have been widely used to identify the differentially expressed genes (DEGs) in systemic lupus erythematosus (SLE). However, the big data from gene microarrays are also challenging to work with in terms of analysis and processing. The presents study combined data from the microarray expression profile (GSE65391) and bioinformatics analysis to identify the key genes and cellular pathways in SLE. Gene ontology (GO) and cellular pathway enrichment analyses of DEGs were performed to investigate significantly enriched pathways. A proteinprotein interaction network was constructed to determine the key genes in the occurrence and development of SLE. A total of 310 DEGs were identified in SLE, including 193 upregulated genes and 117 downregulated genes. GO analysis revealed that the most significant biological process of DEGs was immune system process. Kyoto Encyclopedia of Genes and Genome pathway analysis showed that these DEGs were enriched in signaling pathways associated with the immune system, including the RIGIlike receptor signaling pathway, intestinal immune network for IgA production, antigen processing and presentation and the tolllike receptor signaling pathway. The current study screened the top 10 genes with higher degrees as hub genes, which included 2'5'oligoadenylate synthetase 1, MX dynamin like GTPase 2, interferon induced protein with tetratricopeptide repeats 1, interferon regulatory factor 7, interferon induced with helicase C domain 1, signal transducer and activator of transcription 1, ISG15 ubiquitinlike modifier, DExD/Hbox helicase 58, interferon induced protein with tetratricopeptide repeats 3 and 2'5'oligoadenylate synthetase 2. Module analysis revealed that these hub genes were also involved in the RIGIlike receptor signaling, cytosolic DNAsensing, tolllike receptor signaling and ribosome biogenesis pathways. In addition, these hub genes, from different probe sets, exhibited significant coexpressed tendency in multiexperiment microarray datasets (P<0.01). In conclusion, these key genes and cellular pathways may improve the current understanding of the underlying mechanism of development of SLE. These key genes may be potential biomarkers of diagnosis, therapy and prognosis for SLE.
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Lupus Eritematoso Sistémico/patología , Transcriptoma , Biología Computacional , Regulación de la Expresión Génica , Redes Reguladoras de Genes , Humanos , Lupus Eritematoso Sistémico/genética , Análisis de Secuencia por Matrices de Oligonucleótidos , Mapas de Interacción de Proteínas/genética , Interfaz Usuario-ComputadorRESUMEN
Epigenetic abnormalities play a vital role in the progression of ovarian cancer. Lysine-specific demethylase 1 (LSD1/KDM1A) acts as an epigenetic regulator and is overexpressed in ovarian tumors. However, the upstream regulator of LSD1 expression in this cancer remains elusive. Here, we show that epidermal growth factor (EGF) signaling upregulates LSD1 protein levels in SKOV3 and HO8910 ovarian cancer cells overexpressing both LSD1 and the EGF receptor. This effect is correlated with a decrease in the dimethylation of H3K4, a major substrate of LSD1, in an LSD1-dependent manner. We also show that inhibition of PI3K/AKT, but not MEK, abolishes the EGF-induced upregulation of LSD1 and cell migration, indicating that the PI3K/PDK1/AKT pathway mediates the EGF-induced expression of LSD1 and cell migration. Significantly, LSD1 knockdown or inhibition of LSD1 activity impairs both intrinsic and EGF-induced cell migration in SKOV3 and HO8910 cells. These results highlight a novel mechanism regulating LSD1 expression and identify LSD1 as a promising therapeutic target for treating metastatic ovarian cancer driven by EGF signaling.
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Movimiento Celular/genética , Receptores ErbB/biosíntesis , Histona Demetilasas/genética , Neoplasias Ováricas/genética , Línea Celular Tumoral , Proliferación Celular , Receptores ErbB/genética , Femenino , Regulación Neoplásica de la Expresión Génica/genética , Técnicas de Silenciamiento del Gen , Histona Demetilasas/metabolismo , Humanos , Neoplasias Ováricas/patología , Transducción de Señal/genéticaRESUMEN
To investigate the chemical constituents of Saussurea deltoidea, 10 compounds were isolated from the title plant by various chromatography methods such as silica gel, RP-18 silica gel, Sephadex LH-20 column chromatography, HPLC, et al. Their structures were elucidated by spectral analysis. Five isoprenoids and Five phenylpropanoids were isolated and elucidated as (3R, 6R, 7E) -3-hydroxy-4, 7-megastigmadien-9-one (1), (3S, 5R, 6S, 7E) -5, 6-epoxy-3-hydroxy-7-megastigmen-9-one (2), 3-hydroxy-beta-damascone (3), S-(+) -dehydrovomifoliol (4), megastigman-5-ene-3beta, 9R-diol (5), coniferaldehyde (6), beta-hydroxypropiovanillone (7), 3-hydroxy-1-(4-hydroxy-3, 5-dimethoxyphenyl) -1-propanone (8), dihydrosyringenin (9), 4-[(1S) -3-hydroxy-1-methoxypropyl]-2, 6-dimenthoxyphenol (10). All the compounds were isolated from S. deltoidea for the first time.