Hydrolysis of chitin and chitosans by the human chitinolytic enzymes: chitotriosidase, acidic mammalian chitinase, and lysozyme.

Human chitinolytic enzymes trigger growing interest, not only because a wide range of diseases and allergic responses are linked to chitinous components of pathogens, including their interplay with human enzymes, but also due to the increasing use of chitosans in biomedical applications. Here, we present a detailed side-by-side analysis of the only two human chitinases, chitotriosidase and acidic mammalian chitinase, as well as human lysozyme. By analyzing the cleavage of well-characterized chitosan polymers and defined chitin and chitosan oligomers, we report mild processivity and a quantitative subsite preference typical for GH18 chitinases for chitotriosidase and acidic mammalian chitinase.

Crosstalk between Circulating Tumor Cells and Plasma Proteins-Impact on Coagulation and Anticoagulation.

Cancer metastasis is a complex process. After their intravasation into the circulation, the cancer cells are exposed to a harsh environment of physical and biochemical hazards. Whether circulating tumor cells (CTCs) survive and escape from blood flow defines their ability to metastasize.

Impact of neutrophil extracellular traps on fluid properties, blood flow and complement activation.

Introduction: The intravascular formation of neutrophil extracellular traps (NETs) is a trigger for coagulation and blood vessel occlusion. NETs are released from neutrophils as a response to strong inflammatory signals in the course of different diseases such as COVID-19, cancer or antiphospholipid syndrome. NETs are composed of large, chromosomal DNA fibers decorated with a variety of proteins such as histones.

Key Role of Hyaluronan Metabolism for the Development of Brain Metastases in Triple-Negative Breast Cancer.

Breast cancer (BC) is the second-most common cause of brain metastases (BM) and BCBM patients have a reduced quality of life and a poor prognosis. Hyaluronan (HA), and in particular the hyaluronidase Hyal-1, has been already linked to the development of BCBM, and therefore presents an interesting opportunity to develop new effective therapeutic options. HA metabolism was further discovered by the CRISPR/Cas9-mediated knockout of HYAL1 and the shRNA-mediated down-regulation of HA-receptor CD44 in the brain-seeking triple-negative breast cancer (TNBC) cell line MDA-MB-231-BR.