Tissue inhibitor of metalloproteinase 1 (TIMP-1) promotes plasmablastic differentiation of a Burkitt lymphoma cell line: implications in the pathogenesis of plasmacytic/plasmablastic tumors

Guédez, Liliana; Martı́nez, Antonio; Song, Zhao; Vivero, Angelica; Pittaluga, Stefania; Stetler‐Stevenson, Maryalice; Raffeld, Mark; Stetler‐Stevenson, William G.

doi:10.1182/blood-2004-04-1385

Cited by 42 publications

(42 citation statements)

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“…3 The gene expression profiles of the nongerminal center B-cell-type diffuse large B-cell lymphoma mostly corresponded with those of post-germinal center B-cell cells. 12 However, the immunophenotypes of TIMP-1( þ ) diffuse large B-cell lymphoma were inconsistent with the immunophenotypes of post-germinal center B cells.…”

Section: Discussionmentioning

confidence: 92%

“…23,30 Moreover, it has been shown that upregulation of TIMP-1 expression, in a BL cell line, is related to the activation of STAT3. 3 It has been shown that TIMP-1 is expressed in Reed-Sternberg cells of Hodgkin lymphoma 31,32 and subsets of high grade B-cell lymphoma. 4,5 More recently, the existence of a gray zone between diffuse large B-cell lymphoma and Hodgkin lymphoma has been proposed.…”

Section: Discussionmentioning

confidence: 99%

“…51 In BL cells, overexpression of TIMP-1 leads to the activation and expression of STAT3, and upregulates the expression of BCL-X L , cyclin D2, and CD44. 3,52 Interestingly, BCL-X L is a target protein of activated STAT3 and plays a major role of antiapoptosis. 53 CD44 is also known to promote cell survival by activating the PI-3 kinase/Akt pathway.…”

Section: Discussionmentioning

confidence: 99%

“…A cDNA microarray analysis using TIMP-1 overexpressing Burkitt lymphoma (BL) cell lines revealed that TIMP-1 promotes post-germinal center B-cell differentiation by up-regulating MUM-1 and CD138 and down-regulating BCL6. 3 TIMP-1 expression has been reported in a subset of B-cell lymphoma at the mRNA level 4,5 and has been shown to be associated with a poor clinical outcome in a variety of carcinomas. 6,7 Moreover, TIMP-1 overexpression has been observed in Epstein-Barr virus (EBV) positive lymphoma cell lines.…”

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confidence: 99%

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Clinicopathologic implications of tissue inhibitor of metalloproteinase-1-positive diffuse large B-cell lymphoma

Choi

Lee

et al. 2006

Modern Pathology

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The tissue inhibitor of metalloproteinase-1 (TIMP-1) is a stromal factor that promotes plasmablastic differentiation, and the survival of germinal center B-cells. The expression of TIMP-1 is known to be correlated with a subset of non-Hodgkin lymphoma at the mRNA level, and Epstein-Barr virus infection in vitro. To characterize TIMP-1( þ ) diffuse large B-cell lymphoma, TIMP-1 expression was investigated in tissue microarrays from 182 cases of de novo diffuse large B-cell lymphoma and compared with prognostic factors, immunophenotypes, and Epstein-Barr virus infection status. TIMP-1 was expressed not only in tumor cells themselves, in 14 of 182 cases (8%), designated as TIMP-1( þ ) diffuse large B-cell lymphoma, but also in stromal cells like fibroblasts and endothelial cells. In univariate analysis and hierarchical clustering, our findings suggest that TIMP-1 expression may represent a distinct subgroup. In multivariate analysis, TIMP-1( þ ) diffuse large B-cell lymphoma (n ¼ 14) was associated with unfavorable outcomes compared to TIMP-1(À) diffuse large B-cell lymphoma (n ¼ 168) (odds ratio ¼ 2.5, P ¼ 0.049). Together with TIMP-1 expression, age (greater than 60 years), the presence of B-symptoms, abnormal lactate dehydrogenase level, or more advanced stage (III/IV) was correlated with a poor overall survival. However, TIMP-1 expression in diffuse large B-cell lymphoma was not correlated with other prognostic factors including: clinical stage, international prognostic index score, and nongerminal center B-cell phenotype, as well as Epstein-Barr virus infection. Our results suggest that TIMP-1 expression may be an independent negative prognostic factor in patients with diffuse large B-cell lymphoma.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Clinicopathologic implications of tissue inhibitor of metalloproteinase-1-positive diffuse large B-cell lymphoma

Choi

Lee

et al. 2006

Modern Pathology

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“…Moreover, human recombinant TIMP-1 inhibits the cellmediated cytotoxicity that may play a role in lymphocyte AICD. [16][17][18] These observations prompted the present investigation of the role of TIMP-1 in the development of ALPS and DALD.…”

Section: Introductionmentioning

confidence: 99%

Role of tissue inhibitor of metalloproteinases-1 in the development of autoimmune lymphoproliferation

Boggio¹,

Indelicato²,

Orilieri³

et al. 2010

Haematologica

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BackgroundInherited defects decreasing function of the Fas death receptor cause autoimmune lymphoproliferative syndrome and its variant Dianzani's autoimmune lymphoproliferative disease. Analysis of the lymphocyte transcriptome from a patient with this latter condition detected striking over-expression of osteopontin and tissue inhibitor of metalloproteinases-1. Since previous work on osteopontin had detected increased serum levels in these patients, associated with variations of its gene, the aim of this work was to extend the analysis to tissue inhibitor of metalloproteinases-1. Design and MethodsTissue inhibitor of metalloproteinases-1 levels were evaluated in sera and culture supernatants from patients and controls by enzyme-linked immunosorbent assay. Activation-and Fasinduced cell death were induced, in vitro, using anti-CD3 and anti-Fas antibodies, respectively. ResultsTissue inhibitor of metalloproteinases-1 levels were higher in sera from 32 patients (11 with autoimmune lymphoproliferative syndrome and 21 with Dianzani's autoimmune lymphoproliferative disease) than in 50 healthy controls (P<0.0001), unassociated with variations of the tissue inhibitor of metalloproteinases-1 gene. Both groups of patients also had increased serum levels of osteopontin. In vitro experiments showed that osteopontin increased tissue inhibitor of metalloproteinases-1 secretion by peripheral blood monocytes. Moreover, tissue inhibitor of metalloproteinases-1 significantly inhibited both Fas-and activation-induced cell death of lymphocytes. ConclusionsThese data suggest that high osteopontin levels may support high tissue inhibitor of metalloproteinases-1 levels in autoimmune lymphoproliferative syndrome and Dianzani's autoimmune lymphoproliferative disease, and hence worsen the apoptotic defect in these diseases.Key words: osteopontin, tissue inhibitor of metalloproteinases-1, lymphoproliferation, apoptosis, autoimmunity. Haematologica 2010;95(11):1897-1904 doi:10.3324/haematol.2010 This is an open-access paper. Citation: Boggio E, Indelicato M, Orilieri E, Mesturini R, Mazzarino MC, Campagnoli MF, Ramenghi U, Dianzani U, and Chiocchetti A.Role of tissue inhibitor of metalloproteinases-1 in the development of autoimmune lymphoproliferation. Role of tissue inhibitor of metalloproteinases-1 in the development of autoimmune lymphoproliferation

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Molecular events underlying interleukin‐6 independence in a subclone of the CMA‐03 multiple myeloma cell line

Verdelli

Nobili

Todoerti

et al. 2013

Genes Chromosomes & Cancer

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We explored the molecular mechanisms involved in the establishement of CMA-03/06, an IL-6-independent variant of the multiple myeloma cell line CMA-03 previously generated in our Institution. CMA-03/06 cells grow in the absence of IL-6 with a doubling time comparable with that of CMA-03 cells; neither the addition of IL6 (IL-6) to the culture medium nor co-culture with multipotent mesenchymal stromal cells increases the proliferation rate, although they maintain the responsiveness to IL-6 stimulation as demonstrated by STAT1, STAT3, and STAT5 induction. IL-6 independence of CMA-03/06 cells is not apparently due to the development of an autocrine IL-6 loop, nor to the observed moderate constitutive activation of STAT5 and STAT3, since STAT3 silencing does not affect cell viability or proliferation. When compared to the parental cell line, CMA-03/06 cells showed an activated pattern of the NF-κB pathway. This finding is supported by gene expression profiling (GEP) analysis identifying an appreciable fraction of modulated genes (28/308) in the CMA-03/06 subclone reported to be involved in this pathway. Furthermore, although more resistant to apoptotic stimuli compared to the parental cell line, CMA-03/06 cells display a higher sensibility to NF-κB inhibition induced by bortezomib. Finally, GEP analysis suggests an involvement of a number of cytokines, which might contribute to IL-6 independence of CMA-03/06 by stimulating growth and antiapoptotic processes. In conclusion, the parental cell-line CMA-03 and its variant CMA-03/06 represent a suitable model to further investigate molecular mechanisms involved in the IL-6-independent growth of myeloma cells.

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Tissue inhibitor of metalloproteinase 1 (TIMP-1) promotes plasmablastic differentiation of a Burkitt lymphoma cell line: implications in the pathogenesis of plasmacytic/plasmablastic tumors

Cited by 42 publications

References 40 publications

Clinicopathologic implications of tissue inhibitor of metalloproteinase-1-positive diffuse large B-cell lymphoma

Clinicopathologic implications of tissue inhibitor of metalloproteinase-1-positive diffuse large B-cell lymphoma

Role of tissue inhibitor of metalloproteinases-1 in the development of autoimmune lymphoproliferation

Molecular events underlying interleukin‐6 independence in a subclone of the CMA‐03 multiple myeloma cell line

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