Plasmin inhibitor reduces T-cell lymphoid tumor growth by suppressing matrix metalloproteinase-9-dependent CD11b+/F4/80+ myeloid cell recruitment

α2β1 Integrin Promotes Chemoresistance against Doxorubicin in Cancer Cells through Extracellular Signal-regulated Kinase (ERK)

“…ECM remodeling and degradation by metalloproteinases, which is associated with cancer growth and invasion, is likely to lead to the release of ECM components that can act as "soluble" pep- tides within the tumor microenvironment. T cell malignancies are also associated with metalloproteinases and ECM remodeling as well as dissemination (41)(42)(43)(44). Thus, our study suggests that the ColI released from tissue ECM can bind to ␣2␤1 integrin and provides T-ALL cells with a survival advantage against the cytotoxic effect of doxorubicin.…”

Bone Marrow–Derived CD11b+Jagged2+ Cells Promote Epithelial-to-Mesenchymal Transition and Metastasization in Colorectal Cancer

“…As we do not presently have access to specific monoclonal-neutralizing antibodies to Jag2, we sought to impede the recruitment of CD11b þ cells (which include the Jag2 þ population) into the tumors. Several studies followed a similar approach and concluded that targeting the CD11b þ population of infiltrating cells may be of therapeutic benefit (33,34). Moreover, Toh and colleagues (35) recently showed myeloid-derived suppressor cells (also CD11b þ ) promote EMT, although they did not identify the mechanism involved.…”

New functions of the fibrinolytic system in bone marrow cell-derived angiogenesis

“…Using a T-cell lymphoma model, we showed that genetic Plg deficiency and drug-mediated plasmin blockade delayed T-cell lymphoma growth and diminished MMP-9-dependent CD11b?F4/80? myeloid cell infiltration into lymphoma tissues [71].…”