2026-07-05T14:53:22Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/51212025-05-30T06:26:01Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605col_20.500.12105_19607
Repisalud
author
Bartolome-Izquierdo, Nahikari
author
de Yebenes, Virginia G
author
Alvarez-Prado, Angel Francisco
author
Mur, Sonia M.
author
Lopez, Juan Antonio
author
Roa, Sergio
author
Vazquez, Jesus
author
Ramiro, Almudena R
funder
Ministerio de Economía y Competitividad (España)
funder
Ministerio de Educación, Cultura y Deporte (España)
funder
Unión Europea. Comisión Europea
funder
Unión Europea. Comisión Europea. European Research Council (ERC)
funder
Comunidad Foral de Navarra (España)
funder
Instituto de Salud Carlos III
funder
Fundación La Marató TV3
funder
Fundación ProCNIC
funder
Ministerio de Economía, Industria y Competitividad (España)
2017-10-20T10:23:12Z
2017-10-20T10:23:12Z
2017
Blood. 2017; 129(17):2408-2419
10.1182/blood-2016-08-731166
1528-0020
0006-4971
Blood
28188132
http://hdl.handle.net/20.500.12105/5121
Non-Hodgkin lymphoma comprises a variety of neoplasms, many of which arise from germinal center (GC)-experienced B cells. microRNA-28 (miR-28) is a GC-specific miRNA whose expression is lost in numerous mature B-cell neoplasms. Here we show that miR-28 regulates the GC reaction in primary B cells by impairing class switch recombination and memory B and plasma cell differentiation. Deep quantitative proteomics combined with transcriptome analysis identified miR-28 targets involved in cell-cycle and B-cell receptor signaling. Accordingly, we found that miR-28 expression diminished proliferation in primary and lymphoma cells in vitro. Importantly, miR-28 reexpression in human Burkitt (BL) and diffuse large B-cell lymphoma (DLBCL) xenografts blocked tumor growth, both when delivered in viral vectors or as synthetic, clinically amenable, molecules. Further, the antitumoral effect of miR-28 is conserved in a primary murine in vivo model of BL. Thus, miR-28 replacement is uncovered as a novel therapeutic strategy for DLBCL and BL treatment.
eng
B-CELL LYMPHOMA
NF-KAPPA-B
INDUCED CYTIDINE DEAMINASE
GENOMIC INSTABILITY
BURKITT-LYMPHOMA
CANCER-THERAPY
C-MYC
MICRORNAS
PATHOGENESIS
EXPRESSION
miR-28 regulates the germinal center reaction and blocks tumor growth in preclinical models of non-Hodgkin lymphoma
journal article
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miR-28RegulatesTheGerminal_2017
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SupplementalData_miR-28RegulatesTheGerminal_2017.zip
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miR-28RegulatesTheGerminal_2017.txt