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1.
Clin Transl Oncol ; 21(11): 1580, 2019 11.
Artigo em Inglês | MEDLINE | ID: mdl-31350682

RESUMO

Following the publication of the original article the author listed as Antonio Herrera contacted the Publisher to state that his correct and full name is Antonio Herrera-Merchan. Antonio Herrera-Merchan has agreed to the publication of this erratum.

3.
Clin. transl. oncol. (Print) ; 19(8): 1010-1017, ago. 2017. tab, `bgraf, ilus
Artigo em Inglês | IBECS | ID: ibc-164679

RESUMO

Introduction/purpose. BRG1 is a key regulator of leukemia stem cells. Indeed, it has been observed that this type of cells is unable to divide, survive and develop new tumors when BRG1 is down-regulated. Materials and methods. We assessed BRG1 and miR-155 expression in 23 leukemia cell lines, and two no pathological lymphocyte samples using qPCR. MiR-155 transfection and western blot were used to analyze the relationship between miR-155 and its validated target, BRG1, by measuring protein expression levels. The effect of miR-155 on cell proliferation and prednisolone sensitivity were studied with resazurin assay. Results. BRG1 expression levels could correlate negatively with miR-155 expression levels, at least in Burkitt’s lymphoma and diffuse large B cell lymphoma (DLBCL) cell lines. To clarify the role of miR-155 in the regulation of BRG1 expression, we administrated miR-155 mimics in different leukemia/lymphoma cell lines. Our results suggest that miR-155 regulate negatively and significantly the BRG1 expression at least in the MOLT4 cell line. Conclusion. Our study revealed a previously unknown miR-155 heterogeneity that could result in differences in the treatment with miRNAs in our attempt to inhibit BRG1. However, the expression levels of BRG1 and miR-155, before prednisolone treatment were not statistically significantly associated prednisolone sensitive leukemia cells (AU)


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Assuntos
Humanos , Linhagem Celular Tumoral , MicroRNAs/análise , Prednisolona/uso terapêutico , Leucemia Linfocítica Crônica de Células B/diagnóstico , Leucemia Linfocítica Crônica de Células B/genética , Linfócitos/citologia , Linfócitos/patologia , Linfoma/diagnóstico , Leucemia/diagnóstico , Reação em Cadeia da Polimerase/métodos , Linhagem Celular/citologia , Linhagem Celular/patologia , Western Blotting
4.
Clin Transl Oncol ; 19(8): 1010-1017, 2017 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-28251496

RESUMO

INTRODUCTION/PURPOSE: BRG1 is a key regulator of leukemia stem cells. Indeed, it has been observed that this type of cells is unable to divide, survive and develop new tumors when BRG1 is down-regulated. MATERIALS AND METHODS: We assessed BRG1 and miR-155 expression in 23 leukemia cell lines, and two no pathological lymphocyte samples using qPCR. MiR-155 transfection and western blot were used to analyze the relationship between miR-155 and its validated target, BRG1, by measuring protein expression levels. The effect of miR-155 on cell proliferation and prednisolone sensitivity were studied with resazurin assay. RESULTS: BRG1 expression levels could correlate negatively with miR-155 expression levels, at least in Burkitt's lymphoma and diffuse large B cell lymphoma (DLBCL) cell lines. To clarify the role of miR-155 in the regulation of BRG1 expression, we administrated miR-155 mimics in different leukemia/lymphoma cell lines. Our results suggest that miR-155 regulate negatively and significantly the BRG1 expression at least in the MOLT4 cell line. CONCLUSION: Our study revealed a previously unknown miR-155 heterogeneity that could result in differences in the treatment with miRNAs in our attempt to inhibit BRG1. However, the expression levels of BRG1 and miR-155, before prednisolone treatment were not statistically significantly associated prednisolone sensitive leukemia cells.


Assuntos
Proliferação de Células , DNA Helicases/metabolismo , Regulação Neoplásica da Expressão Gênica , Leucemia/patologia , Linfoma/patologia , MicroRNAs/genética , Proteínas Nucleares/metabolismo , Fatores de Transcrição/metabolismo , DNA Helicases/genética , Humanos , Leucemia/genética , Leucemia/metabolismo , Linfoma/genética , Linfoma/metabolismo , Proteínas Nucleares/genética , Fatores de Transcrição/genética , Células Tumorais Cultivadas
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