B cell differentiation in EBV-positive Burkitt Lymphoma is impaired at post-transcriptional level by miRNA altered expression

E Leucci; A Onnis; M Cocco; G De Falco; F Imperatore; G Antonicelli; V Costanzo; G Cerino; S Mannucci; R Cantisani; J Nyagol; W Mwanda; R Iriso; M Owang; K Schurfeld; C Bellan; S Lazzi; L Leoncini

doi:10.1002/ijc.24655

B cell differentiation in EBV-positive Burkitt Lymphoma is impaired at post-transcriptional level by miRNA altered expression

E Leucci, A Onnis, M Cocco, G De Falco, F Imperatore, G Antonicelli, V Costanzo, G Cerino, S Mannucci, R Cantisani, J Nyagol, W Mwanda, R Iriso, M Owang, K Schurfeld, C Bellan, S Lazzi, L Leoncini

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

68 Citationer (Scopus)

Abstract

Udgivelsesdato: 2009-Jun-15

Originalsprog	Engelsk
Tidsskrift	International Journal of Cancer
ISSN	0020-7136
DOI	https://doi.org/10.1002/ijc.24655
Status	Udgivet - 2009

Adgang til dokumentet

10.1002/ijc.24655

Citationsformater

Leucci, E., Onnis, A., Cocco, M., De Falco, G., Imperatore, F., Antonicelli, G., Costanzo, V., Cerino, G., Mannucci, S., Cantisani, R., Nyagol, J., Mwanda, W., Iriso, R., Owang, M., Schurfeld, K., Bellan, C., Lazzi, S., & Leoncini, L. (2009). B cell differentiation in EBV-positive Burkitt Lymphoma is impaired at post-transcriptional level by miRNA altered expression. International Journal of Cancer. https://doi.org/10.1002/ijc.24655

Leucci, E, Onnis, A, Cocco, M, De Falco, G, Imperatore, F, Antonicelli, G, Costanzo, V, Cerino, G, Mannucci, S, Cantisani, R, Nyagol, J, Mwanda, W, Iriso, R, Owang, M, Schurfeld, K, Bellan, C, Lazzi, S & Leoncini, L 2009, 'B cell differentiation in EBV-positive Burkitt Lymphoma is impaired at post-transcriptional level by miRNA altered expression', International Journal of Cancer. https://doi.org/10.1002/ijc.24655

@article{c46a20d0662b11de8bc9000ea68e967b,

title = "B cell differentiation in EBV-positive Burkitt Lymphoma is impaired at post-transcriptional level by miRNA altered expression",

abstract = "Endemic, sporadic and HIV-associated Burkitt lymphoma (BL) all have a B-cell phenotype and a MYC translocation, but a variable association with the Epstein-Barr virus (EBV). However, there is still no satisfactory explanation of how EBV participates in the pathogenesis of BL. A recent investigation suggested that EBV-positive and EBV-negative BL have different cells of origin. In particular, according to immunoglobulin gene mutation analysis, EBV-negative BLs may originate from early centroblasts, whereas EBV-positive BLs appear to arise from postgerminal center B cells or memory B cells. The appearance of a germinal center phenotype in EBV-positive cells might thus derive from a block in B cell differentiation. The exit from the germinal center involves a complex series of events which require the activation of BLIMP-1 and the consequent down-regulation of several target genes.Here, we investigated the expression of specific miRNAs predicted to be involved in B cell differentiation and we found that hsa-miR-127 is differentially expressed between EBV-positive and EBV-negative BLs. In particular, it was strongly up-regulated only in EBV-positive BL samples, whereas EBV-negative cases showed levels of expression similar to normal controls, including microdissected GC cells.In addition, we found evidence that hsa-miR-127 is involved in B cell differentiation process through post transcriptional regulation of BLIMP1 and XBP1. The over-expression of this miRNA may thus represent a key event in the lymphomagenesis of EBV positive BL, by blocking the B cell differentiation process. (c) 2009 UICC.",

author = "E Leucci and A Onnis and M Cocco and {De Falco}, G and F Imperatore and G Antonicelli and V Costanzo and G Cerino and S Mannucci and R Cantisani and J Nyagol and W Mwanda and R Iriso and M Owang and K Schurfeld and C Bellan and S Lazzi and L Leoncini",

year = "2009",

doi = "10.1002/ijc.24655",

language = "English",

journal = "International Journal of Cancer",

issn = "0020-7136",

publisher = "JohnWiley & Sons, Inc.",

}

TY - JOUR

T1 - B cell differentiation in EBV-positive Burkitt Lymphoma is impaired at post-transcriptional level by miRNA altered expression

AU - Leucci, E

AU - Onnis, A

AU - Cocco, M

AU - De Falco, G

AU - Imperatore, F

AU - Antonicelli, G

AU - Costanzo, V

AU - Cerino, G

AU - Mannucci, S

AU - Cantisani, R

AU - Nyagol, J

AU - Mwanda, W

AU - Iriso, R

AU - Owang, M

AU - Schurfeld, K

AU - Bellan, C

AU - Lazzi, S

AU - Leoncini, L

PY - 2009

Y1 - 2009

N2 - Endemic, sporadic and HIV-associated Burkitt lymphoma (BL) all have a B-cell phenotype and a MYC translocation, but a variable association with the Epstein-Barr virus (EBV). However, there is still no satisfactory explanation of how EBV participates in the pathogenesis of BL. A recent investigation suggested that EBV-positive and EBV-negative BL have different cells of origin. In particular, according to immunoglobulin gene mutation analysis, EBV-negative BLs may originate from early centroblasts, whereas EBV-positive BLs appear to arise from postgerminal center B cells or memory B cells. The appearance of a germinal center phenotype in EBV-positive cells might thus derive from a block in B cell differentiation. The exit from the germinal center involves a complex series of events which require the activation of BLIMP-1 and the consequent down-regulation of several target genes.Here, we investigated the expression of specific miRNAs predicted to be involved in B cell differentiation and we found that hsa-miR-127 is differentially expressed between EBV-positive and EBV-negative BLs. In particular, it was strongly up-regulated only in EBV-positive BL samples, whereas EBV-negative cases showed levels of expression similar to normal controls, including microdissected GC cells.In addition, we found evidence that hsa-miR-127 is involved in B cell differentiation process through post transcriptional regulation of BLIMP1 and XBP1. The over-expression of this miRNA may thus represent a key event in the lymphomagenesis of EBV positive BL, by blocking the B cell differentiation process. (c) 2009 UICC.

AB - Endemic, sporadic and HIV-associated Burkitt lymphoma (BL) all have a B-cell phenotype and a MYC translocation, but a variable association with the Epstein-Barr virus (EBV). However, there is still no satisfactory explanation of how EBV participates in the pathogenesis of BL. A recent investigation suggested that EBV-positive and EBV-negative BL have different cells of origin. In particular, according to immunoglobulin gene mutation analysis, EBV-negative BLs may originate from early centroblasts, whereas EBV-positive BLs appear to arise from postgerminal center B cells or memory B cells. The appearance of a germinal center phenotype in EBV-positive cells might thus derive from a block in B cell differentiation. The exit from the germinal center involves a complex series of events which require the activation of BLIMP-1 and the consequent down-regulation of several target genes.Here, we investigated the expression of specific miRNAs predicted to be involved in B cell differentiation and we found that hsa-miR-127 is differentially expressed between EBV-positive and EBV-negative BLs. In particular, it was strongly up-regulated only in EBV-positive BL samples, whereas EBV-negative cases showed levels of expression similar to normal controls, including microdissected GC cells.In addition, we found evidence that hsa-miR-127 is involved in B cell differentiation process through post transcriptional regulation of BLIMP1 and XBP1. The over-expression of this miRNA may thus represent a key event in the lymphomagenesis of EBV positive BL, by blocking the B cell differentiation process. (c) 2009 UICC.

U2 - 10.1002/ijc.24655

DO - 10.1002/ijc.24655

M3 - Journal article

C2 - 19530237

SN - 0020-7136

JO - International Journal of Cancer

JF - International Journal of Cancer

ER -