Wen Jin Wu

TL;DR: It is reported that Ca2+ depletion induces E-cadherin ubiquitination and lysosomal degradation and that Cdc42 plays an important role in regulating this process, and it is found that GTP-dependent binding of CDC42 to E- cadher in is critical for C dc42 to induce the dissolution of adherens junctions.

TL;DR: It is reported that trastuzumab significantly alters the expression of myocardial genes essential for DNA repair, cardiac and mitochondrial functions, which is associated with impaired left ventricular performance in mice coupled with significant ultrastructural alterations in cardiomyocytes revealed by electron microscopy.

TL;DR: It is shown that Cdc42 and c-Cbl are critical components involved in the regulation of EGFR protein levels and that restoration of proper EGFR degradation by disrupting CDC42 regulation of c- Cbl can reduce cell proliferation and migration in MDA-MB-231 and BT20 cells.

TL;DR: The novel role of DNA topoisomerase IIB as a shared target for enhanced cardiotoxicity induced by trastuzumab and anthracyclines-based combination regimens is discussed, and the potential impact of trastzumab intervention in immune checkpoint inhibitors-based therapies is speculated.

TL;DR: A comprehensive overview of the current knowledge on the cardiotoxicity of trastuzumab is given, primarily focusing on data from clinical trials and highlighting the main molecular mechanisms proposed.