2) Involvement of ROS and oxidative stress in cancer Most cancer cells exhibit elevated oxidative stress with increased metabolic activity and production of ROS. The main goal is to study at the molecular level how does the cell sense oxidative stress and which mechanisms are triggered to allow adaptation to the stress. We, therefore, are trying to identify and characterize the components and mechanisms which activate signal transduction pathways to respond to oxidative stress in the colon and ovarian cancer.
Cell adhesion molecules take part in intercellular and cell-extracellular matrix interactions of cancer. Cancer progression is a multi-step process in which some adhesion molecules play a pivotal role in the development of recurrent, invasive, and distant metastasis. A growing body of evidence indicates that alterations in the adhesion properties of neoplastic cells play a pivotal role in the development and progression of cancer. Epithelial cell adhesion molecule (EpCAM) was initially discovered as a cell-surface antigen highly expressed in a variety of carcinomas. In our previous work, we identified EpCAM acts as a potent inhibitor of novel protein kinase C (nPKC) in cancer cells via a short segment of the EpCAM cytoplasmic tail. We showed that the loss of EpCAM causes sequentially a strong overstimulation of PKC activity and of the Erk pathway, leading to exacerbated myosin contractility, loss of cadherin-mediated adhesion, tissue dissociation, and, ultimately, cell death.