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Chinese Journal of Oncology ; (12): 742-746, 2011.
Artículo en Chino | WPRIM | ID: wpr-320147

RESUMEN

<p><b>OBJECTIVE</b>To elucidate the regulatory mechanism underlying proliferation and anti-apoptosis in NSCLC by overexpression of miR-21.</p><p><b>METHODS</b>Real-time PCR was used to measure miR-21 abundance in non-small cell lung cancer (NSCLC) tumor samples and adjacent normal tissues, as well as NSCLC cell lines. Tumor suppressor genes as potential targets of miR-21 were predicted by sequence analysis. Luciferase assay and Western blot were used to assess the regulatory effect. The effect on A549 cell viability and apoptosis by miR-21-induced gene repression was tested by trypan-blue exclusion and flow cytometry.</p><p><b>RESULTS</b>miR-21 expression was 2.24-fold higher in the NSCLC tumor samples and 3.06-fold higher in the A549 cells than that in the adjacent normal tissues. Sequence prediction and gene expression regulation assays showed that miR-21 could reversely regulate the expression of PDCD4 (P < 0.01). Suppression of miR-21 expression is associated with an elevation of Pdcd4, resulting in a significant reduction of proliferation and the apoptosis rate (2.6%) was increased to 10.9%. Moreover, the anti-proliferation and pro-apoptotic effect by miR-21 suppression could be reversed by PDCD4 knock down.</p><p><b>CONCLUSION</b>Suppression of the tumor suppressor PDCD4 expression may be one of the important regulatory pathways of the miR-21-mediated cell proliferation and decrease of apoptosis in non-small cell lung cancer.</p>


Asunto(s)
Anciano , Humanos , Masculino , Persona de Mediana Edad , Apoptosis , Proteínas Reguladoras de la Apoptosis , Genética , Metabolismo , Carcinoma de Pulmón de Células no Pequeñas , Metabolismo , Patología , Línea Celular Tumoral , Proliferación Celular , Regulación Neoplásica de la Expresión Génica , Neoplasias Pulmonares , Metabolismo , Patología , MicroARNs , Genética , Metabolismo , Oligonucleótidos Antisentido , Genética , Interferencia de ARN , Proteínas de Unión al ARN , Genética , Metabolismo , Transfección
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