Tumor hypoxia evidences the differential regulation of Mdm2-p53 axis by PTEN in tumor derived vs. normal endothelial cells.

Hypoxia, a condition of oxygen tension lower than physiological level, plays a crucial role in shaping the tumor microenvironment and modulates distinct cell populations activity. The tumor suppressor PTEN regulates angiogenesis, a process involving endothelial cells (ECs). Pathological in tumors, it is crucial for growth.

Microenvironment commits breast tumor ECs to dedifferentiation by micro-RNA-200-b-3p regulation and extracellular matrix remodeling.

Hypoxia shapes the tumor microenvironment, modulates distinct cell population activities, and activates pathological angiogenesis in cancer, where endothelial cells (ECs) are the most important players. This study aimed to evidence the influences of the tumor microenvironment on the global gene expression pattern characteristic for ECs and the distinct responses displayed by tumor-derived ECs in comparison to the healthy endothelium during endothelial to mesenchymal transition (EndMT) and its regulation by miR-200-b-3p. Immortalized lines of ECs from the same patient with breast cancer, healthy breast tissue (HBH.