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miR-181b functions as an oncomiR in colorectal cancer by targeting PDCD4
Protein & Cell ; (12): 722-734, 2016.
Article en En | WPRIM | ID: wpr-757383
Biblioteca responsable: WPRO
ABSTRACT
Programmed cell death 4 (PDCD4) is a RNA-binding protein that acts as a tumor suppressor in many cancer types, including colorectal cancer (CRC). During CRC carcinogenesis, PDCD4 protein levels remarkably decrease, but the underlying molecular mechanism for decreased PDCD4 expression is not fully understood. In this study, we performed bioinformatics analysis to identify miRNAs that potentially target PDCD4. We demonstrated miR-181b as a direct regulator of PDCD4. We further showed that activation of IL6/STAT3 signaling pathway increased miR-181b expression and consequently resulted in downregulation of PDCD4 in CRC cells. In addition, we investigated the biological effects of PDCD4 inhibition by miR-181b both in vitro and in vivo and found that miR-181b could promote cell proliferation and migration and suppress apoptosis in CRC cells and accelerate tumor growth in xenograft mice, potentially through targeting PDCD4. Taken together, this study highlights an oncomiR role for miR-181b in regulating PDCD4 in CRC and suggests that miR-181b may be a novel molecular therapeutic target for CRC.
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Texto completo: 1 Base de datos: WPRIM Asunto principal: Patología / ARN Neoplásico / Neoplasias Colorrectales / Proteínas de Unión al ARN / Ratones SCID / Células CACO-2 / MicroARNs / Proliferación Celular / Proteínas Reguladoras de la Apoptosis / Xenoinjertos Tipo de estudio: Prognostic_studies Límite: Animals / Humans / Male Idioma: En Revista: Protein & Cell Año: 2016 Tipo del documento: Article
Texto completo: 1 Base de datos: WPRIM Asunto principal: Patología / ARN Neoplásico / Neoplasias Colorrectales / Proteínas de Unión al ARN / Ratones SCID / Células CACO-2 / MicroARNs / Proliferación Celular / Proteínas Reguladoras de la Apoptosis / Xenoinjertos Tipo de estudio: Prognostic_studies Límite: Animals / Humans / Male Idioma: En Revista: Protein & Cell Año: 2016 Tipo del documento: Article