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1.
J Cell Mol Med ; 24(10): 5842-5849, 2020 05.
Artículo en Inglés | MEDLINE | ID: mdl-32285560

RESUMEN

Metabolic reprogramming has become a hot topic recently in the regulation of tumour biology. Although hundreds of altered metabolic genes have been reported to be associated with tumour development and progression, the important prognostic role of these metabolic genes remains unknown. We downloaded messenger RNA expression profiles and clinicopathological data from The Cancer Genome Atlas and the Gene Expression Omnibus database to uncover the prognostic role of these metabolic genes. Univariate Cox regression analysis and lasso Cox regression model were utilized in this study to screen prognostic associated metabolic genes. Patients with high-risk demonstrated significantly poorer survival outcomes than patients with low-risk in the TCGA database. Also, patients with high-risk still showed significantly poorer survival outcomes than patients with low-risk in the GEO database. What is more, gene set enrichment analyses were performed in this study to uncover significantly enriched GO terms and pathways in order to help identify potential underlying mechanisms. Our study identified some survival-related metabolic genes for rectal cancer prognosis prediction. These genes might play essential roles in the regulation of metabolic microenvironment and in providing significant potential biomarkers in metabolic treatment.


Asunto(s)
Genes Relacionados con las Neoplasias , Neoplasias del Recto/genética , Neoplasias del Recto/metabolismo , Bases de Datos Genéticas , Regulación hacia Abajo/genética , Perfilación de la Expresión Génica , Regulación Neoplásica de la Expresión Génica , Ontología de Genes , Humanos , Análisis Multivariante , Pronóstico , Modelos de Riesgos Proporcionales , Reproducibilidad de los Resultados , Factores de Riesgo , Análisis de Supervivencia , Regulación hacia Arriba/genética
2.
Int J Clin Exp Pathol ; 8(6): 6779-85, 2015.
Artículo en Inglés | MEDLINE | ID: mdl-26261562

RESUMEN

This study was aimed to evaluate the effect of Angelica Sinensis on experimental rat models in which spinal cord injury was induced by studying different factors. Different factors causing inflammation play a key role in pathophysiology of SCI. Here three groups of rats (n=15, each was used). These included a sham control group where only laminectomy was performed, SCI group where SCI was induced and AS/SCI group where although SCI was induced but Angelica Sinensis was also administered to study its effect and draw a comparison with control. The expression of I-kBα and NF-kB p65 was also studied using western blotting and after recording optical density (OD) values of western blots. MPO activity was used to measure the effect of 20 mg/kg Angelica Sinensis. The levels of proinflammatory cytokines TNF-α, IL-1ß and IL-6 were also studied. As compared with SCI group and sham control it was observed that Angelica Sinensis significantly reduced the expression of I-kBα and NF-kB p65, (P<0.05), while MPO activity was also significantly reduced. Proinflammatory cytokine level was also reduced in treated group as compared to both other groups. On the basis of this study we concluded that the use of 20 mg/kg Angelica Sinensis in rat models can attenuate the secondary damage caused by SCI and thus help in controlling the pathology of SCI in rats.


Asunto(s)
Angelica sinensis , Antiinflamatorios/farmacología , Medicamentos Herbarios Chinos/farmacología , Mielitis/prevención & control , Traumatismos de la Médula Espinal/tratamiento farmacológico , Médula Espinal/efectos de los fármacos , Angelica sinensis/química , Animales , Antiinflamatorios/aislamiento & purificación , Citocinas/metabolismo , Modelos Animales de Enfermedad , Medicamentos Herbarios Chinos/aislamiento & purificación , Proteínas I-kappa B/metabolismo , Mediadores de Inflamación/metabolismo , Masculino , Mielitis/metabolismo , Mielitis/patología , Inhibidor NF-kappaB alfa , Peroxidasa/metabolismo , Fitoterapia , Plantas Medicinales , Ratas Sprague-Dawley , Médula Espinal/metabolismo , Médula Espinal/patología , Traumatismos de la Médula Espinal/metabolismo , Traumatismos de la Médula Espinal/patología , Factor de Transcripción ReIA/metabolismo
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