Matrix MetalloProteinases (MMPs) andTissue Inhibitors of MetalloProteinases (TIMPs): positive and negative regulators intumor cell adhesion
By D. Bourboulia, W. Stetler-Stevenson. Seminars in Cancer Biology, 2010
702 citations recorded by the source corpus.
Cells adhere to one another and/or to matrices that surround them. Regulation of cell-cell (intercellular) and cell-matrix adhesion is tightly controlled in normal cells, however, defects in cell adhesion are common in the majority of humancancers. Multilateral communication among tumor cells with the extracellular matrix (ECM) and neighbor cells is accomplished through adhesion molecules, ECM components, proteolytic enzymes and their endogenous inhibitors. There is sufficient evidence to suggest that reduced adherence is a tumor cell propertyengaged during tumor progression. Tumor cells acquire the ability to change shape, detach and easily move through spaces disorganizing the normal tissue architecture. This property is due to changes in expression levels of adhesion molecules and/or due to elevated levels of secreted proteolytic enzymes, including matrix metalloproteinases (MMPs). Among other roles, MMPsdegrade the ECMand, therefore, prepare the path for tumor cells to migrate, invade and spread to distant secondary areas, where they form metastasis. Tissue Inhibitors of Metalloproteinases or TIMPs control MMP activities and, therefore, minimize matrix degradation. Both MMPs and TIMPs are involved in tissue remodeling and decisively regulate tumor cell progression including tumor angiogenesis. In this review, we describe and discuss data that support the important role of MMPs and TIMPs in cancer cell adhesion and tumor progression.
Subfields: Cancer Research, Immunology and Allergy, Oncology
View Paper: https://www.semanticscholar.org/paper/86860c14b823426d0ad8ab2b7353cc297487801f
Citations in the corpus
- Extracellular matrix (ECM) stiffness and degradation as cancer drivers (2018, background): “MMPs cleave ECM to make a path for cancer cells to modify their shape and to attain proliferative, invasiveness and migratory features.(4) Dynamin 2, Src kinase and Cdc42 are involved in regulation of invadopodia assembly and function.”