Expression of surface-associated 82kDa-proMMP-9 in primary acute leukemia blast cells inversely correlates with patients' risk

Expression of a specific extracellular matrix signature is a favorable prognostic factor in acute myeloid leukemia

“…Owing to the scarcity of data about ECM and AML, it is difficult to discuss the individual roles of the ECM genes in the specific signature. It seems, nevertheless, notable that two of the three up-regulated genes characterizing the ECM high phenotype have been already implicated in AML: MMP9 , in fact, has been already recently described as generally down-regulated in AML [13] , and its higher expression postulated to be a positive factor in patients’ prognosis [17] , thus completely matching our observation. Intriguingly, we also observe significant up-regulation of ELANE , the neutrophils’ elastase, in these patients.…”

Effects of nano-encapsulated curcumin-chrysin on telomerase, MMPs and TIMPs gene expression in mouse B16F10 melanoma tumour model

“…MMPs, matrix metalloproteinase enzyme family, play a key role in the proteolytic degradation of ECM and, therefore, cancer cells metastasis [34,48]. MMP-9 and MMP-2 are the members of this family that increase invasion of the tumour [49].…”

An extracellular matrix signature in leukemia precursor cells and acute myeloid leukemia

“…CD44 belongs to a family of transmembrane glycoproteins whose primary function is to bind hyaluronic acid (HA), laminins, collagens, matrix metalloproteinases (MMPs), osteopontin, etc., 12 and this receptor has previously been implicated in cell migration, proliferation, differentiation, survival, and bone marrow homing of hematopoietic stem/progenitor cells as well as in the homing of LSCs to intra-and extra-medullary niches and in resistance to chemotherapy. 12 We observed that the leukemic precursors with a higher expression of CD44 (the group of cells we called "definitive leukemic cells") also exhibit a parallel upregulation of genes whose products interact directly (COL4A5, LAMB2) 9,10 or indirectly (MMP2, COL18A1) 12 with CD44 and downregulation of MMP9 (which directly interacts with CD44 but whose levels correlate inversely with patient prognosis), 13 suggesting that the establishment of a "CD44-ECM network", rather than the expression of CD44 alone, is a crucial step in the progression of leukemic cells towards an aggressive phenotype. This also seems to be supported by the observation that, in two independent cohorts, patients with an ECM profile similar to that of the definitive leukemic cells showed significantly shorter survival (overall and endpoint), independently from well-known karyotypical or molecular drivers of AML.…”