MEC1 and MEC2: two new cell lines derived from B-chronic lymphocytic leukaemia in prolymphocytoid transformation

Stacchini, Alessandra; Aragno, M.; Vallario, Antonella; Alfarano, A; Circosta, Paola; Gottardi, Daniela; Faldella, A.; Rege‐Cambrin, Giovanna; Thunberg, Ulf; Nilsson, Kenneth; Caligaris-Cappio, Federico

doi:10.1016/s0145-2126(98)00154-4

Cited by 248 publications

(249 citation statements)

References 24 publications

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“…Here, we used MEC1 cells (a CLL cell line derived from a patient undergoing prolymphocytoid transformation; ref. 39) and show that Lck siRNA reduces the expression of LCK but has no effect on the expression of Lyn in these cells (Fig. 4E).…”

Section: Sirna-mediated Reduction Of Lck Expression In Cll Cells Redumentioning

confidence: 84%

LCK Is an Important Mediator of B-Cell Receptor Signaling in Chronic Lymphocytic Leukemia Cells

Talab

Allen

Thompson

et al. 2013

Molecular Cancer Research

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B-cell receptor (BCR) signals promote survival of chronic lymphocytic leukemia (CLL) cells, and it is believed that overexpressed and constitutively active Lyn mediates this signaling. Here, we show that CLL cells express lymphocyte-specific protein tyrosine kinase (LCK) and that inhibition of this Src family tyrosine kinase with the specific inhibitor [4-amino-5-(4-phenoxyphenyl)-7H-pyrrolo[3,2-d]pyrimidin-7-yl-cyclopentane (Lck-i)], or reduction of its expression with siRNA, blocks the induction of CD79a, Syk, inhibitor of IkB kinase (IKK), Akt, and extracellular signal-regulated kinase (ERK) phosphorylation by BCR cross-linking in these cells. Furthermore, we show that CLL cells with high levels of LCK expression have higher levels of BCR-mediated IKK, Akt, and ERK phosphorylation as well as cell survival than CLL cells with low levels of LCK expression. We also show that treatment of CLL cells with Lck-i inhibits BCR cross-linking-induced cell survival. Taken together, these data show a major role for LCK in proximal and distal BCR-mediated signaling in CLL cells and suggest that LCK expression is important in the pathogenesis of this disease. On a clinical level, these studies advocate the use of specific LCK inhibitors in the treatment of progressive CLL. Mol Cancer Res; 11(5); 541-54. Ó2013 AACR.

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Section: Sirna-mediated Reduction Of Lck Expression In Cll Cells Redumentioning

confidence: 84%

LCK Is an Important Mediator of B-Cell Receptor Signaling in Chronic Lymphocytic Leukemia Cells

Talab

Allen

Thompson

et al. 2013

Molecular Cancer Research

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“…The resulting B cell population was Ͼ92% CD19 ϩ and Ͼ72% CD5 ϩ , determined on a Coulter Epics XL flow cytometer (Beckman Coulter, Fullerton, CA). The MEC-1 cell line, established from a B-CLL patient (23), was obtained from Dr. Enrique Ocio (Cancer Research Center, Salamanca, Spain) and maintained in IMDM medium (Lonza, Basel, Switzerland), 10% fetal bovine serum. K562 and K562-␣4 cells were obtained from Dr. Joaquín Teixidó (Centro de Investigaciones Biológicas, Madrid) and cultured in RPMI 1640, 10% fetal bovine serum.…”

Section: Methodsmentioning

confidence: 99%

A 17-residue Sequence from the Matrix Metalloproteinase-9 (MMP-9) Hemopexin Domain Binds α4β1 Integrin and Inhibits MMP-9-induced Functions in Chronic Lymphocytic Leukemia B Cells

Ugarte-Berzal

Bailón

Amigo-Jiménez

et al. 2012

Journal of Biological Chemistry

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“…CLL cell line MEC1 44 was cultured in RPMI 1640 medium supplemented with 10% fetal bovine serum (FBS; Sigma-Aldrich), 4 mM glutamine…”

Section: Supplemental Materialsmentioning

confidence: 99%

ANGPT2promoter methylation is strongly associated with gene expression and prognosis in chronic lymphocytic leukemia

et al. 2013

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MEC1 and MEC2: two new cell lines derived from B-chronic lymphocytic leukaemia in prolymphocytoid transformation

Cited by 248 publications

References 24 publications

LCK Is an Important Mediator of B-Cell Receptor Signaling in Chronic Lymphocytic Leukemia Cells

LCK Is an Important Mediator of B-Cell Receptor Signaling in Chronic Lymphocytic Leukemia Cells

A 17-residue Sequence from the Matrix Metalloproteinase-9 (MMP-9) Hemopexin Domain Binds α4β1 Integrin and Inhibits MMP-9-induced Functions in Chronic Lymphocytic Leukemia B Cells

ANGPT2promoter methylation is strongly associated with gene expression and prognosis in chronic lymphocytic leukemia

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