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HS1 has a central role in the trafficking and homing of leukemic B cells.

Scielzo, Cristina, Bertilaccio, Maria T. S., Simonetti, Giorgia, Dagklis, Antonis, ten Hacken, Elisa, Fazi, Claudia, Muzio, Marta, Caiolfa, Valeria, Kitamura, Daisuke, Restuccia, Umberto, Bachi, Angela, Rocchi, Martina, Ponzoni, Maurilio, Ghia, Paolo, Caligaris-Cappio, Federico·2010·Blood
DOI 10.1182/blood-2009-12-258814
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Abstract

The function of the intracellular protein hematopoietic cell–specific Lyn substrate-1 (HS1) in B lymphocytes is poorly defined. To investigate its role in migration, trafficking, and homing of leukemic B lymphocytes we have used B cells from HS1−/− mice, the HS1-silenced human chronic lymphocytic leukemia (CLL) MEC1 cell line and primary leukemic B cells from patients with CLL. We have used both in vitro and in vivo models and found that the lack of expression of HS1 causes several important functional effects. In vitro, we observed an impaired cytoskeletal remodeling that resulted in diminished cell migration, abnormal cell adhesion, and increased homotypic aggregation. In vivo, immunodeficient Rag2−/−γc−/− mice injected with HS1-silenced CLL B cells showed a decreased organ infiltration with the notable exception of the bone marrow (BM). The leukemic-prone Eμ-TCL1 transgenic mice crossed with HS1-deficient mice were compared with Eμ-TCL1 mice and showed an earlier disease onset and a reduced survival. These findings show that HS1 is a central regulator of cytoskeleton remodeling that controls lymphocyte trafficking and homing and significantly influences the tissue invasion and infiltration in CLL.

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Research works printed but not linked: 38

  1. Kitamura, 1989, Isolation and characterization of a novel human gene expressed specifically in the cells of hematopoietic lineage., Nucleic Acids Res, 17, 9367
  2. Fischer, 2005, Expression of the gene for hematopoietic cell specific protein is not restricted to cells of hematopoietic origin., Int J Mol Med, 15, 611
  3. Hao, 2005, The coiled-coil domain is required for HS1 to bind to F-actin and activate Arp2/3 complex., J Biol Chem, 280, 37988, 10.1074/jbc.M504552200 · DOI
  4. Takemoto, 1996, Distinct binding patterns of HS1 to the Src SH2 and SH3 domains reflect possible mechanisms of recruitment and activation of downstream molecules., Int Immunol, 8, 1699, 10.1093/intimm/8.11.1699 · DOI
  5. Gomez, 2006, HS1 functions as an essential actin-regulatory adaptor protein at the immune synapse., Immunity, 24, 741, 10.1016/j.immuni.2006.03.022 · DOI
  6. Carrizosa, 2009, Hematopoietic lineage cell-specific protein 1 is recruited to the immunological synapse by IL-2-inducible T cell kinase and regulates phospholipase Cgamma1 Microcluster dynamics during T cell spreading., J Immunol, 183, 7352, 10.4049/jimmunol.0900973 · DOI
  7. Butler, 2008, Differently phosphorylated forms of the cortactin homolog HS1 mediate distinct functions in natural killer cells., Nat Immunol, 9, 887, 10.1038/ni.1630 · DOI
  8. Brunati, 2005, Thrombin-induced tyrosine phosphorylation of HS1 in human platelets is sequentially catalyzed by Syk and Lyn tyrosine kinases and associated with the cellular migration of the protein., J Biol Chem, 280, 21029, 10.1074/jbc.M412634200 · DOI
  9. Taniuchi, 1995, Antigen-receptor induced clonal expansion and deletion of lymphocytes are impaired in mice lacking HS1 protein, a substrate of the antigen-receptor-coupled tyrosine kinases., EMBO J, 14, 3664, 10.1002/j.1460-2075.1995.tb00036.x · DOI
  10. Yamanashi, 1997, Role of tyrosine phosphorylation of HS1 in B cell antigen receptor-mediated apoptosis., J Exp Med, 185, 1387, 10.1084/jem.185.7.1387 · DOI
  11. Hao, 2004, Syk-mediated tyrosine phosphorylation is required for the association of hematopoietic lineage cell-specific protein 1 with lipid rafts and B cell antigen receptor signalosome complex., J Biol Chem, 279, 33413, 10.1074/jbc.M313564200 · DOI
  12. Scielzo, 2005, HS1 protein is differentially expressed in chronic lymphocytic leukemia patient subsets with good or poor prognoses., J Clin Invest, 115, 1644, 10.1172/JCI24276 · DOI
  13. Muzio, 2007, HS1 complexes with cytoskeleton adapters in normal and malignant chronic lymphocytic leukemia B cells., Leukemia, 21, 2067, 10.1038/sj.leu.2404744 · DOI
  14. Ghia, 2008, Microenvironmental influences in chronic lymphocytic leukaemia: the role of antigen stimulation., J Intern Med, 264, 549, 10.1111/j.1365-2796.2008.02030.x · DOI
  15. Caligaris-Cappio, 2008, Novel insights in chronic lymphocytic leukemia: are we getting closer to understanding the pathogenesis of the disease?, J Clin Oncol, 26, 4497, 10.1200/JCO.2007.15.4393 · DOI
  16. Richardson, 2006, ZAP-70 expression is associated with enhanced ability to respond to migratory and survival signals in B-cell chronic lymphocytic leukemia (B-CLL)., Blood, 107, 3584, 10.1182/blood-2005-04-1718 · DOI
  17. Lopez-Giral, 2004, Chemokine receptors that mediate B cell homing to secondary lymphoid tissues are highly expressed in B cell chronic lymphocytic leukemia and non-Hodgkin lymphomas with widespread nodular dissemination., J Leukoc Biol, 76, 462, 10.1189/jlb.1203652 · DOI
  18. Stark, 1984, Anomalous function of vimentin in chronic lymphocytic leukemia lymphocytes., Blood, 63, 415, 10.1182/blood.V63.2.415.bloodjournal632415 · DOI
  19. Caligaris-Cappio, 1986, Cytoskeleton organization is aberrantly rearranged in the cells of B chronic lymphocytic leukemia and hairy cell leukemia., Blood, 67, 233, 10.1182/blood.V67.1.233.233 · DOI
  20. Ramsay, 2008, Chronic lymphocytic leukemia T cells show impaired immunological synapse formation that can be reversed with an immunomodulating drug., J Clin Invest, 118, 2427
  21. Bichi, 2002, Human chronic lymphocytic leukemia modeled in mouse by targeted TCL1 expression., Proc Natl Acad Sci U S A, 99, 6955, 10.1073/pnas.102181599 · DOI · Paper page
  22. Mulligan, 2009, Lymphocytes, B lymphocytes, and clonal CLL cells: observations on the impact of the new diagnostic criteria in the 2008 Guidelines for Chronic Lymphocytic Leukemia (CLL)., Blood, 113, 6496, 10.1182/blood-2008-07-166710 · DOI
  23. Stacchini, 1999, MEC1 and MEC2: two new cell lines derived from B-chronic lymphocytic leukaemia in prolymphocytoid transformation., Leuk Res, 23, 127, 10.1016/S0145-2126(98)00154-4 · DOI
  24. Seminario, 2008, Signal initiation in T-cell receptor microclusters., Immunol Rev, 221, 90, 10.1111/j.1600-065X.2008.00593.x · DOI
  25. Trautmann, 2005, Microclusters initiate and sustain T cell signaling., Nat Immunol, 6, 1213, 10.1038/ni1205-1213 · DOI
  26. Ilani, 2009, T cell antigen receptor signaling and immunological synapse stability require myosin IIA., Nat Immunol, 10, 531, 10.1038/ni.1723 · DOI
  27. Mattila, 2008, Filopodia: molecular architecture and cellular functions., Nat Rev Mol Cell Biol, 9, 446, 10.1038/nrm2406 · DOI
  28. Depoil, 2008, CD19 is essential for B cell activation by promoting B cell receptor-antigen microcluster formation in response to membrane-bound ligand., Nat Immunol, 9, 63, 10.1038/ni1547 · DOI
  29. Schuuring, 1998, Characterization of the EMS1 gene and its product, human Cortactin., Cell Adhes Commun, 6, 185, 10.3109/15419069809004475 · DOI
  30. Lai, 2009, Cortactin promotes migration and platelet-derived growth factor-induced actin reorganization by signaling to Rho-GTPases., Mol Biol Cell, 20, 3209, 10.1091/mbc.e08-12-1180 · DOI
  31. Bertilaccio, 2010, A novel Rag2−/−gammac−/−-xenograft model of human CLL., Blood, 115, 1605, 10.1182/blood-2009-05-223586 · DOI
  32. Kaplan, 2005, VEGFR1-positive haematopoietic bone marrow progenitors initiate the pre-metastatic niche., Nature, 438, 820, 10.1038/nature04186 · DOI · Paper page
  33. Lwin, 2009, Lymphoma cell adhesion-induced expression of B cell-activating factor of the TNF family in bone marrow stromal cells protects non-Hodgkin's B lymphoma cells from apoptosis., Leukemia, 23, 170, 10.1038/leu.2008.266 · DOI
  34. Johnson, 2006, Characterization of the TCL-1 transgenic mouse as a preclinical drug development tool for human chronic lymphocytic leukemia., Blood, 108, 1334, 10.1182/blood-2005-12-011213 · DOI · Paper page
  35. Huang, 2007, T-cell-receptor-dependent actin regulatory mechanisms., J Cell Sci, 120, 723, 10.1242/jcs.000786 · DOI
  36. Yokoyama, 2008, Inhibitory receptors signal activation., Immunity, 29, 515, 10.1016/j.immuni.2008.09.009 · DOI
  37. Burkhardt, 2008, The actin cytoskeleton in T cell activation., Annu Rev Immunol, 26, 233, 10.1146/annurev.immunol.26.021607.090347 · DOI
  38. Hartmann, 2009, Circulating B-cell chronic lymphocytic leukemia cells display impaired migration to lymph nodes and bone marrow., Cancer Res, 69, 3121, 10.1158/0008-5472.CAN-08-4136 · DOI · Paper page

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Metadata

Authors
Scielzo, C., Bertilaccio, M. T. S., Simonetti, G., Dagklis, A., ten Hacken, E., Fazi, C., Muzio, M., Caiolfa, V., Kitamura, D., Restuccia, U., Bachi, A., Rocchi, M., Ponzoni, M., Ghia, P., & Caligaris-Cappio, F.
Affiliations
  • Unit of Lymphoid Malignancies, Division of Molecular Oncology, San Raffaele Scientific Institute, Milano, Italy;
  • Unit of B Cell Neoplasia, Division of Molecular Oncology, San Raffaele Scientific Institute, Milano, Italy;
  • Unit of Dynamic Fluorescence Spectroscopy, Division of Molecular Oncology,
  • Division of Molecular Biology, Research Institute for Biological Sciences, Tokyo University of Science, Tokyo, Japan;
  • Università degli Studi di Milano, Milano, Italy;
  • Biomolecular Mass Spectrometry Unit, Division of Genetics and Cell Biology,
  • Pathology Unit, Division of Molecular Oncology, San Raffaele Scientific Institute, Milano, Italy;
Venue
Blood
Publisher
American Society of Hematology
Published
2010-11-04
Volume
116
Issue
18
Pages
3537-3546
ISSN
  • 0006-4971
  • 1528-0020
DOI
10.1182/blood-2009-12-258814
Cited by
74
References
0
Language
en

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CoChat. (2026). Citation check: HS1 has a central role in the trafficking and homing of leukemic B cells. https://app.cochat.ai/papers/10.1182/blood-2009-12-258814
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Scielzo, C., Bertilaccio, M. T. S., Simonetti, G., Dagklis, A., ten Hacken, E., Fazi, C., Muzio, M., Caiolfa, V., Kitamura, D., Restuccia, U., Bachi, A., Rocchi, M., Ponzoni, M., Ghia, P., & Caligaris-Cappio, F. (2010). HS1 has a central role in the trafficking and homing of leukemic B cells. Blood. https://doi.org/10.1182/blood-2009-12-258814