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1.
Int J Mol Sci ; 22(16)2021 Aug 04.
Artículo en Inglés | MEDLINE | ID: mdl-34445094

RESUMEN

Idiopathic pulmonary fibrosis (IPF) is a refractory interstitial lung disease for which there is no effective treatment. Although the pathogenesis of IPF is not fully understood, TGF-ß and epithelial-mesenchymal transition (EMT) have been shown to be involved in the fibrotic changes of lung tissues. Kurarinone is a prenylated flavonoid isolated from Sophora Flavescens with antioxidant and anti-inflammatory properties. In this study, we investigated the effect of kurarinone on pulmonary fibrosis. Kurarinone suppressed the TGF-ß-induced EMT of lung epithelial cells. To assess the therapeutic effects of kurarinone in bleomycin (BLM)-induced pulmonary fibrosis, mice were treated with kurarinone daily for 2 weeks starting 7 days after BLM instillation. Oral administration of kurarinone attenuated the fibrotic changes of lung tissues, including accumulation of collagen and improved mechanical pulmonary functions. Mechanistically, kurarinone suppressed phosphorylation of Smad2/3 and AKT induced by TGF-ß1 in lung epithelial cells, as well as in lung tissues treated with BLM. Taken together, these results suggest that kurarinone has a therapeutic effect on pulmonary fibrosis via suppressing TGF-ß signaling pathways and may be a novel drug candidate for pulmonary fibrosis.


Asunto(s)
Flavonoides/uso terapéutico , Fibrosis Pulmonar/tratamiento farmacológico , Transducción de Señal/efectos de los fármacos , Factor de Crecimiento Transformador beta/metabolismo , Animales , Bleomicina , Línea Celular , Transición Epitelial-Mesenquimal , Flavonoides/farmacología , Humanos , Masculino , Ratones Endogámicos BALB C , Fibrosis Pulmonar/inducido químicamente , Fibrosis Pulmonar/metabolismo , Fibrosis Pulmonar/patología
2.
J Med Internet Res ; 22(7): e17031, 2020 07 30.
Artículo en Inglés | MEDLINE | ID: mdl-32729838

RESUMEN

BACKGROUND: The health behaviors of young adults lag behind those of other age groups, and active health management is needed to improve health behaviors and prevent chronic diseases. In addition, developing good lifestyle habits earlier in life could reduce the risk of metabolic syndrome (MetS) later on. OBJECTIVE: The aim of this study is to investigate the effects of the e-Motivate4Change program, for which health apps and wearable devices were selected based on user needs. The program was developed for the prevention and management of MetS in young adults. METHODS: This experimental study used a nonequivalent control group. In total, 59 students from 2 universities in Daegu, Korea participated in the study (experimental group n=30; control group n=29). Data were collected over 4 months, from June 1 to September 30, 2018. The experimental group received a 12-week e-Motivate4Change program intervention, and the control group received MetS education and booklets without the e-Motivate4Change program intervention. RESULTS: After the program, the experimental group had significantly higher scores for health-related lifestyle (t=3.86; P<.001) and self-efficacy (t=6.00; P<.001) than did the control group. Concerning BMI, there were significant effects by group (F=1.01; P<.001) and for the group × time interaction (F=4.71; P=.034). Concerning cholesterol, there were significant main effects for group (F=4.32; P=.042) and time (F=9.73; P<.001). CONCLUSIONS: The e-Motivate4Change program effectively improved participants' health-related lifestyle scores and self-efficacy, and significantly reduced their BMI and cholesterol levels. The program can be used to identify and prevent MetS among young adults.


Asunto(s)
Síndrome Metabólico/terapia , Aplicaciones Móviles/normas , Telemedicina/métodos , Dispositivos Electrónicos Vestibles/normas , Femenino , Humanos , Masculino , Ensayos Clínicos Controlados no Aleatorios como Asunto , Adulto Joven
3.
Stud Health Technol Inform ; 310: 1466-1467, 2024 Jan 25.
Artículo en Inglés | MEDLINE | ID: mdl-38269699

RESUMEN

This study was aimed to identify knowledge structure and trends in severe COVID-19 risk factor using text network analysis. The 22,628 papers published during from January 2020 to December 2021. We analyzed and visualized using Text Rank analyzer and Gephi software. They were grouped into 5 central themes - biomedical factors, occupational environmental factors, demographic factors, health behavior factors, and complications. The emerging topics were identified to the chronological trends. This study can promote a systematic understanding of severe COVID-19 risk factors.


Asunto(s)
COVID-19 , Humanos , Conductas Relacionadas con la Salud , Conocimiento , Factores de Riesgo , Programas Informáticos
4.
Tumour Biol ; 33(3): 731-8, 2012 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-22373580

RESUMEN

KLK6 encoding kallikrein-related peptidase 6, a trypsin-like serine protease, has been shown to be upregulated in several cancers, although the tumorigenic role of KLK6 has not been elucidated. In this study, KLK6 was identified as a highly upregulated gene in gastric cancer; therefore, the possibility that KLK6 might be a suitable candidate tumor marker was examined. RT-PCR and immunohistochemical analysis showed overexpression of KLK6 in gastric cancer tissues compared to nontumor regions. Sera from gastric cancer patients had a 1.7-fold increase in KLK6 (373.1 µg/L, P = 0.048) compared to healthy individuals (214.2 µg/L), although there was no significant difference among patients with various tumor stages. Cellular invasiveness decreased by 45% in cells transfected with KLK6-specific small interfering RNA. Exogenous overexpression of KLK6 led to decreased activity of the E-cadherin promoter. This study shows that KLK6 is significantly upregulated and secreted in gastric cancer tissues and sera, suggesting that KLK6 might be used as a potential biomarker and therapeutic target for gastric cancer.


Asunto(s)
Regulación Neoplásica de la Expresión Génica , Calicreínas/genética , Calicreínas/metabolismo , Neoplasias Gástricas/enzimología , Neoplasias Gástricas/genética , Cadherinas/genética , Línea Celular Tumoral , Humanos , Invasividad Neoplásica/genética , Regiones Promotoras Genéticas , ARN Mensajero/metabolismo , Activación Transcripcional , Regulación hacia Arriba/genética
5.
Cancer ; 117(12): 2608-19, 2011 Jun 15.
Artículo en Inglés | MEDLINE | ID: mdl-21656738

RESUMEN

BACKGROUND: Kallikrein-related peptidase 6 (KLK6) encodes a trypsin-like serine protease that is up-regulated in several cancers, although the putative functions of KLK6 in cancer have not been elucidated. In the current study, overexpression of KLK6 was identified in colon cancer, and the possibility that KLK6 may be a suitable candidate as a tumor marker was examined. METHODS: Messenger RNA (mRNA) transcript levels and protein up-regulation of KLK6 in colon cancer tissues was examined using reverse transcriptase-polymerase chain reaction, immunohistochemistry, and clinicopathologic analyses. Cell proliferation, invasiveness, and antiapoptotic activity were determined in colon cancer cells that were transfected with small-interfering RNA (siRNA) of KLK6. RESULTS: KLK6 mRNA was up-regulated significantly in tumor tissues compared with nontumor regions. KLK6 protein was strongly expressed in adenocarcinomas but was not expressed in normal mucosa or in premalignant dysplastic lesions. Sera from patients with colon cancer revealed an increase in KLK6 secretion (0.25 µg/mL; P = .031) compared with noncancer cells (0.19 µg/mL). Clinicopathologic and immunohistochemical studies of 143 patients with colon cancer revealed a significant correlation between KLK6 expression and Dukes disease stage (P = .005). High KLK6 expression was associated significantly with shorter overall (P = .001) and recurrence-free survival (P = .001). The rates of proliferation and invasiveness were decreased by 50% in cells that were transfected with KLK6 siRNA. The overexpression of KLK6 led to decreased activity of the E-cadherin promoter. CONCLUSIONS: KLK6 was up-regulated significantly in tissues and sera from patients with colon cancer and was associated closely with a poor prognosis, suggesting that KLK6 may be used as a potential biomarker and a therapeutic target for colon cancer.


Asunto(s)
Neoplasias del Colon/enzimología , Calicreínas/fisiología , Adulto , Anciano , Línea Celular Tumoral , Colon/enzimología , Neoplasias del Colon/mortalidad , Neoplasias del Colon/patología , Femenino , Humanos , Calicreínas/análisis , Calicreínas/genética , Masculino , Persona de Mediana Edad , Invasividad Neoplásica , Estadificación de Neoplasias , Pronóstico , Modelos de Riesgos Proporcionales , ARN Mensajero/análisis , Regulación hacia Arriba
6.
Phytomedicine ; 80: 153392, 2021 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-33113503

RESUMEN

BACKGROUND: Acacetin 7-O-ß-D-glucoside (tilianin) is a major constituent of Agastache rugosa, a traditional medicine that has long been used for the treatment of gastrointestinal disorders. Tilianin has a wide variety of pharmacological properties such as cardioprotective, neuroprotective, and anti-atherogenic activities. We recently discovered that tilianin has the ability to suppress MUC5AC expression in vitro. In addition, we have established an in vivo model of allergic asthma using house dust mite (HDM) that can be applied to tilianin. PURPOSE: We investigated the effects of tilianin on airway inflammation in a HDM-induced asthma mouse model and associated mechanisms. METHODS: Tilianin was treated in splenocytes cultured in Th0 condition and HDM-stimulated bone marrow-derived dendritic cells (BMDCs), and their mRNA expression and cytokines production were determined by quantitative real-time PCR and ELISA. To evaluate the effects of tilianin in an allergic asthma model, mice were sensitized and challenged with HDM. Tilianin was administered prior to challenge by oral gavage and airway hyper-reactivity (AHR) to methacholine, inflammatory cell infiltration, cytokine levels, and airway remodeling were assessed. RESULTS: Tilianin inhibited the production of Th2-related cytokines in splenocytes, which play pivotal roles in allergic airway inflammation. When treated in HDM-stimulated BMDCs, tilianin decreased Th2-skewing cytokine IL-33 and transcription factor IRF4. On the contrary, tilianin increased Th1-skewing regulators, IL-12 and IRF1. In an HDM-induced asthmatic mouse model, tilianin attenuated AHR and airway inflammation. Tilianin suppressed the expression of Th2-related cytokines, IL-13 and IL-33 in lung tissues. As seen in HDM-stimulated BMDCs, tilianin also downregulated the expression of the transcription factor IRF4 but not IRF1. CONCLUSION: Taken together, these results suggest that tilianin attenuates HDM-induced allergic airway inflammation by inhibiting Th2-mediated inflammation through the selective inhibition of the IRF4-IL-33 axis in dendritic cells.


Asunto(s)
Antiasmáticos/farmacología , Asma/tratamiento farmacológico , Flavonoides/farmacología , Glicósidos/farmacología , Factores Reguladores del Interferón/metabolismo , Células Th2/efectos de los fármacos , Remodelación de las Vías Aéreas (Respiratorias) , Animales , Asma/inmunología , Asma/metabolismo , Citocinas/metabolismo , Células Dendríticas/efectos de los fármacos , Células Dendríticas/inmunología , Modelos Animales de Enfermedad , Regulación hacia Abajo/efectos de los fármacos , Femenino , Hipersensibilidad/tratamiento farmacológico , Hipersensibilidad/etiología , Factores Reguladores del Interferón/inmunología , Interleucina-33/metabolismo , Pulmón/efectos de los fármacos , Pulmón/inmunología , Pulmón/metabolismo , Ratones Endogámicos BALB C , Pyroglyphidae/patogenicidad , Células Th2/inmunología , Células Th2/metabolismo
7.
Clin Chim Acta ; 415: 12-9, 2013 Jan 16.
Artículo en Inglés | MEDLINE | ID: mdl-22975528

RESUMEN

BACKGROUND: Carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) inhibits anoikis and affects the malignant phenotype of cancer cells. In this study, we analyzed CEACAM6 as a gene that is highly upregulated in colon cancer tissues, and examined the assertion that CEACAM6 might be a suitable candidate tumor marker for the diagnosis of colon cancer. METHODS: CEACAM6 gene expression in human colon tissues was performed by tissue microarray and analyzed using RT-PCR (each of normal and tumor tissue, n=40) and immunohistochemical and clinicopathological (colon cancer patients, n=143) analyses. RESULTS: CEACAM6 transcriptional and translational levels were significantly upregulated in human tumor tissues compared to non-tumor regions, and clinicopathological analysis revealed a significant correlation between CEACAM6 protein expression and Dukes' stage (p<0.001). High expression levels of CEACAM6 were significantly associated with lower overall survival (p<0.001) and shorter recurrence-free survival (p<0.001). We demonstrated that knockdown of CEACAM6 with CEACAM6-specific small interfering RNA in colorectal cancer cells attenuated invasivity (35%); conversely, the overexpression of CEACAM6 increased invasiveness. CONCLUSIONS: CEACAM6 is significantly upregulated in colon cancer tissues and is closely associated with poor prognosis, indicating that CEACAM6 might be used as a tumor biomarker and a potential therapeutic target for colon cancer.


Asunto(s)
Adenocarcinoma/genética , Adenocarcinoma/patología , Antígenos CD/genética , Biomarcadores de Tumor/genética , Moléculas de Adhesión Celular/genética , Neoplasias Colorrectales/genética , Neoplasias Colorrectales/patología , Regulación Neoplásica de la Expresión Génica , Adenocarcinoma/diagnóstico , Adenocarcinoma/mortalidad , Adulto , Anciano , Biomarcadores de Tumor/antagonistas & inhibidores , Moléculas de Adhesión Celular/antagonistas & inhibidores , Línea Celular Tumoral , Neoplasias Colorrectales/diagnóstico , Neoplasias Colorrectales/mortalidad , Femenino , Proteínas Ligadas a GPI/antagonistas & inhibidores , Proteínas Ligadas a GPI/genética , Silenciador del Gen , Humanos , Masculino , Persona de Mediana Edad , Invasividad Neoplásica , Análisis de Secuencia por Matrices de Oligonucleótidos , Pronóstico , ARN Interferente Pequeño/genética , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Análisis de Supervivencia
8.
BMB Rep ; 43(5): 349-54, 2010 May.
Artículo en Inglés | MEDLINE | ID: mdl-20510019

RESUMEN

Previously, we reported that overexpression of Opa (Neisseria gonorrhoeae opacity-associated)-interacting protein 5 (OIP5) caused multi-septa formation and growth defects, both of which are considered cancer-related phenotypes. To evaluate OIP5 as a possible cancer therapeutic target, we examined its expression level in 66 colorectal cancer patients. OIP5 was upregulated about 3.7-fold in tumors and over 2-fold in 58 out of 66 colorectal cancer patients. Knockdown of OIP5 expression by small interfering RNA specific to OIP5 (siOIP5) resulted in growth inhibition of colorectal and gastric cancer cell lines. Growth inhibition of SNU638 by siOIP5 caused an increase in sub-G1 DNA content, as measured by flow cytometry, as well as an apoptotic gene expression profile. These results indicate that knockdown of OIP5 may induce apoptosis in cancer cells. Therefore, we suggest that OIP5 might be a potential cancer therapeutic target, although the mechanisms of OIP5-induced carcinogenesis should be elucidated.


Asunto(s)
Proteínas Cromosómicas no Histona/metabolismo , Neoplasias Colorrectales/metabolismo , Neoplasias Gástricas/metabolismo , Animales , Apoptosis , Proteínas de Ciclo Celular , Proteínas Cromosómicas no Histona/genética , Neoplasias Colorrectales/genética , Neoplasias Colorrectales/patología , Neoplasias Colorrectales/terapia , Perfilación de la Expresión Génica , Humanos , Análisis por Micromatrices , ARN Interferente Pequeño/genética , ARN Interferente Pequeño/metabolismo , Neoplasias Gástricas/genética , Neoplasias Gástricas/patología , Neoplasias Gástricas/terapia , Regulación hacia Arriba
9.
J Cancer Res Clin Oncol ; 135(6): 761-9, 2009 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-19034516

RESUMEN

PURPOSE: CKS2 was identified as an upregulated gene in gastric cancer via our DNA microarray. This study was to verify the upregulation of CKS2 in many gastric cancer patients and to examine the CKS2-mediated cellular response. METHODS: CKS2 upregulation was analyzed using reverse transcriptase PCR, real-time PCR, and immunohistochemical and clinicopathological analyses. GFP-CKS2 or CKS2-siRNA was used to analyze the cellular localization and proliferation. RESULTS: The strong upregulation of mRNA and protein levels of CKS2 was identified. In CKS2-overexpressing cells, tumor suppressor p53 and p21(cip1) were downregulated and cell growth was increased. In contrast, CKS2-siRNA-transfected cells showed an increased tumor suppressor expression and decreased cell growth. CONCLUSIONS: We showed that CKS2 was significantly upregulated in gastric cancers and a high level of CKS2 was highly correlated with histologic tumor differentiation and pathological grade of the tumor size, lymph node, and metastasis stage. We suggest that the cell cycle regulator CKS2 might be deeply involved in gastric cancer progression.


Asunto(s)
Proteínas Portadoras/genética , Proteínas de Ciclo Celular/genética , Proliferación Celular , Proteínas Quinasas/genética , Neoplasias Gástricas/patología , Western Blotting , Quinasas CDC2-CDC28 , Proteínas Portadoras/metabolismo , Proteínas de Ciclo Celular/metabolismo , Línea Celular Tumoral , Femenino , Regulación Neoplásica de la Expresión Génica , Proteínas Fluorescentes Verdes/genética , Proteínas Fluorescentes Verdes/metabolismo , Humanos , Inmunohistoquímica , Masculino , Microscopía Confocal , Persona de Mediana Edad , Proteínas Quinasas/metabolismo , ARN Interferente Pequeño/genética , Proteínas Recombinantes de Fusión/genética , Proteínas Recombinantes de Fusión/metabolismo , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Neoplasias Gástricas/genética , Neoplasias Gástricas/metabolismo , Transcripción Genética , Transfección , Proteína p53 Supresora de Tumor/genética , Proteína p53 Supresora de Tumor/metabolismo , Regulación hacia Arriba
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