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MicroRNA-191在T淋巴母细胞性白血病/淋巴瘤中的表达及其作用机制研究

OBJECTIVE: To evaluate the correlation between MicroRNA-191 (miR-191) and T lymphoblastic leukemia/lymphoma (T-ALL/LBL) to probe its underlying molecular mechanism. METHODS: The expression of miR-191 was examined by real-time PCR (RT-PCR) in 20 T-ALL/LBL tissue samples and 20 lymphoid reactive hyper...

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Detalles Bibliográficos
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Editorial office of Chinese Journal of Hematology 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7343091/
https://www.ncbi.nlm.nih.gov/pubmed/27093985
http://dx.doi.org/10.3760/cma.j.issn.0253-2727.2016.04.003
Descripción
Sumario:OBJECTIVE: To evaluate the correlation between MicroRNA-191 (miR-191) and T lymphoblastic leukemia/lymphoma (T-ALL/LBL) to probe its underlying molecular mechanism. METHODS: The expression of miR-191 was examined by real-time PCR (RT-PCR) in 20 T-ALL/LBL tissue samples and 20 lymphoid reactive hyperplasia (LRH) tissue samples. The correlation between miR-191 and the clinicopathological feature of T-ALL/LBL was analyzed. Antisense miR-191 lentiviral vectors was constructed and transfected into T-ALL/LBL Jukat cells. After transfection, the expression of miR-191was examined by RT-PCR. The cell activity was evaluated by CCK-8 asssy. The cell cycle and apoptosis were determined by flow cytometry. RESULTS: Compared with LRH samples, the results of RT-PCR showed significant upregulation of miR-191 in 20 T-ALL/LBL tissue samples (1.875±0.079 vs 1.000, P<0.05). The expression level of miR-191 was negatively associated with prognosis. Compared with LV-NC-GFP and control groups, the expression of miR-191 significantly decreased after transfection of antisense miR-191 lentiviral vectors (0.578±0.012 vs 1.011±0.053 and 1.000, P<0.05), the percentages of apoptotic cells and the cell in G(0)/G(1) phase significantly increased (P<0.05). CONCLUSION: miR-191 might play a significant role in the development of T-ALL/LBL, implicating a new target for therapy.