Cysteine cathepsins: multifunctional enzymes in cancer

By M. Mohamed, Bonnie F. Sloane. Nature Reviews. Cancer, 2006

1,248 citations recorded by the source corpus.

Subfields: Cancer Research, Oncology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/470020e747be414d3247b2c909838c8930484f1a

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Citations in the corpus

Tumor‐associated macrophages (TAM) as major players of the cancer‐related inflammation (2009, background): “Regarding the specific influence on tumor microenvironment, TAM abundantly secrete matrix proteins and several proteases such as serine proteases, MMPs, and cathepsins, which act on cell–cell junctions, modify the ECM composition, and promote basal membrane disruption [110–113].”
Cysteine cathepsins: From structure, function and regulation to new frontiers (2011, background): “Despite the important role of cathepsins from tumor cells, there is an increasing body of evidence confirming the up-regulation of cysteine cathepsins by cells of the tumor microenvironment, such as macrophages [302, 340, 341] .”
Accessories to the crime: functions of cells recruited to the tumor microenvironment. (2012, positive): “…growth factors, can selectively cleave cell-cell and cell-ECM adhesion molecules, and/or ECM molecules (ligands for the latter), thereby disabling growth suppressing adhesion complexes maintaining homeostasis (Lu et al., 2011a; Mohamed and Sloane, 2006; Pontiggia et al., 2011; Xu et al., 2009).”
Bicarbonate Increases Tumor pH and Inhibits Spontaneous Metastases (2009, background): “Thus, it seems that the acid pHe of tumors can induce the release of this protease that is involved in extracellular matrix turnover in breast cancer (44).”
Extracellular matrix structure. (2016, background): “In the intracellular milieu, cysteine cathepsins also degrade ECM proteins such as collagens, taken up into phagosomes via uPAR/pro-uPA complexes [317].”
Extracellular matrix dynamics in development and regenerative medicine (2008, background): “The proteolytic cleavage of ECM components represents another mechanism by which the ECM is remodeled and, when misregulated, results in a number of disease states (Koblinski et al., 2000; Mohamed and Sloane, 2006).”
Epithelial-mesenchymal transition in cancer metastasis: mechanisms, markers and strategies to overcome drug resistance in the clinic. (2009, background): “Interestingly, MMPs have been found upregulated in EMT cells [47] but also capable of inducing EMT [48].”
Emerging roles of proteases in tumour suppression (2007, background): “We now recognize that proteolytic enzymes contribute to all stages of tumour progression, and not only to the later stages as was originally though”
Differential Macrophage Programming in the Tumor Microenvironment (2012, positive): “This activity has been directly demonstrated in vitro [73, 74] and in vivo with mice genetically deficient for cathepsin B, cathepsin S and urokinase/plasminogen activator (uPA), all of which derive primarily from TAMs in the tumor microenvironment [75–77].”
Lysosomal positioning coordinates cellular nutrient responses (2011, background): “For example, increased mTORC1 activity and decreased autophagy are associated with tumorigenesis, and lysosomal spreading is associated with metastasi”