Increased angiogenesis in chronic lymphocytic leukemia (CLL) is linked to advanced disease, with CLL cells showing a pro-angiogenic gene expression pattern influenced by their environment.
MMP-9, a component of the microenvironment, was found to enhance MMP-9 expression and secretion in CLL cells, leading to increased endothelial cell proliferation.
MMP-9 also altered the expression of angiogenic-related genes, particularly decreasing TSP-1 and increasing VEGF, by involving specific molecular pathways, highlighting its role in CLL pathology.
MMP-9 plays a significant role in the pathology of Chronic Lymphocytic Leukemia (CLL) by regulating cell survival, migration, and inducing cell arrest when expressed at high levels.
A study identified that MMP-9 alters the gene expression of specific genes in CLL cells, notably including CD99, which affects cell adhesion and migration.
The research highlights CD99 as a new therapeutic target that, when influenced by MMP-9, regulates CLL cell behavior and could lead to new treatment strategies.
Researchers found that MMP-9, when overexpressed, hinders the movement of chronic lymphocytic leukemia (CLL) cells, leading to studies on a mutant form of MMP-9 that doesn't break down proteins (MMP-9MutE).
In mouse models, these MMP-9MutE cells showed reduced ability to migrate to key areas like the spleen and bone marrow compared to control cells.
The study identified changes in cellular signaling pathways; MMP-9MutE cells had higher levels of PTEN and lower p-ERK, indicating that non-proteolytic functions of MMP-9 are important in CLL cell migration and may affect disease progression.
CLL is currently an incurable disease, but arsenic trioxide (ATO) shows promise as an effective therapy by inducing cell death in CLL cells.
ATO affects gene expression related to oxidative stress, notably increasing the levels of the gene HMOX1 and the protein MMP-9, which are involved in the response to treatment.
HMOX1 has a pro-apoptotic role that enhances the cytotoxic effects of ATO, making it a potential new therapeutic target when combined with ATO for CLL treatment.