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Downregulated miR-17, miR-29c, miR-92a and miR-214 may be related to BCL11B overexpression in T cell acute lymphoblastic leukemia.
He, Zifan; Liao, Ziwei; Chen, Shaohua; Li, Bo; Yu, Zhi; Luo, Gengxin; Yang, Lijian; Zeng, Chengwu; Li, Yangqiu.
Afiliação
  • He Z; Key Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, School of Medicine, Jinan University, Guangzhou, China.
  • Liao Z; Key Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, School of Medicine, Jinan University, Guangzhou, China.
  • Chen S; Key Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, School of Medicine, Jinan University, Guangzhou, China.
  • Li B; Key Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, School of Medicine, Jinan University, Guangzhou, China.
  • Yu Z; Department of Hematology, First Affiliated Hospital, Jinan University, Guangzhou, China.
  • Luo G; Department of Hematology, First Affiliated Hospital, Jinan University, Guangzhou, China.
  • Yang L; Key Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, School of Medicine, Jinan University, Guangzhou, China.
  • Zeng C; Key Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, School of Medicine, Jinan University, Guangzhou, China.
  • Li Y; Key Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, School of Medicine, Jinan University, Guangzhou, China.
Asia Pac J Clin Oncol ; 14(5): e259-e265, 2018 Oct.
Article em En | MEDLINE | ID: mdl-29749698
ABSTRACT

AIM:

BCL11B overexpression is a characteristic of most T cell acute lymphoblastic leukemia (T-ALL) cases, and downregulated BCL11B in leukemic T cells inhibits cell proliferation and induces apoptosis. The purpose of this study was to analyze the miRNA expression pattern that may be related to BCL11B regulation in T-ALL.

METHODS:

Quantitative real-time PCR was used to detect the miRNAs miR-17-3p, miR-17-5p, miR-29c-3p, miR-92a-3p, miR-214-3p and miR-214-5p, the BCL11B expression level in peripheral blood mononuclear cells which was obtained from 17 de novo and untreated T-ALL patients, and 15 healthy individuals (HIs) served as control. Correlations between the relative miRNA expression levels and BCL11B were analyzed.

RESULTS:

Based on the computational prediction that certain miRNAs bind the BCL11B 3'-UTR, miR-17-3p, miR-17-5p, miR-29c-3p, miR-92a-3p, miR-214-3p and miR-214-5p were found to be candidates for regulating BCL11B. The expression levels of the six miRNAs were decreased compared with HIs, and with the exception of miR-17-5p, statistically significant differences in expression levels were found in the T-ALL group. Moreover, while significantly higher BCL11B expression was found in the T-ALL group, a negative trend in the correlation level for all six miRNAs could be found in all groups; however, statistical significance was only found for miR-214-3p in the T-ALL group.

CONCLUSION:

miRNA downregulation together with BCL11B upregulation suggests that miR-17, miR-29c, miR-92a and miR-214 might be involved in BCL11B regulation. The therapeutic promise of regulating the expression of these miRNAs for T-ALL therapy may be considered in the future.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Proteínas Repressoras / Regulação Neoplásica da Expressão Gênica / Proteínas Supressoras de Tumor / Leucemia-Linfoma Linfoblástico de Células T Precursoras Tipo de estudo: Prognostic_studies Limite: Adolescent / Adult / Child / Female / Humans / Male / Middle aged Idioma: En Ano de publicação: 2018 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Proteínas Repressoras / Regulação Neoplásica da Expressão Gênica / Proteínas Supressoras de Tumor / Leucemia-Linfoma Linfoblástico de Células T Precursoras Tipo de estudo: Prognostic_studies Limite: Adolescent / Adult / Child / Female / Humans / Male / Middle aged Idioma: En Ano de publicação: 2018 Tipo de documento: Article