Accepted Abstracts: J Cancer Sci Ther
Conversely to normal cells, where deregulated oxidative stress drives the activation of death pathways, malignant cells exploit oxidative milieu for their advantage. Cancer cells are located in a very complex microenvironment together with stromal components that participate to enhance oxidative stress to promote tumor progression. Tumor cells engage a key relationship with cancer associated fibroblasts (CAFs), behaving as active participants in tumor progression, by eliciting in cancer cells epithelial mesenchymal transition (EMT) and enhancing stem cells traits and metastatic dissemination. This reciprocal interplay between CAFs and cancer cells goes beyond the engagement of EMT, including mutual metabolic reprogramming. Indeed, cancer cells allocate Warburg metabolism to their corrupted stromal CAFs and exploit their byproducts to grow in glucose free environment, symbiotically adapting with its stromal cells to glucose availability. Our studies are aimed at understanding the interplay among tumor microenvironment, oxidative stress and metabolic reprogramming of cancer cells, recently defined by Hanahan and Weinberg as new ?hallmarks of cancer?. We identified in miR200 family a potential molecular link among these events, and involved this family of miRNAs in oxidants handling by cancer cells, in sirtuins regulation and nutrient sensing, as well as in EMT induced by stromal CAFs.
Paola Chiarugi is Full Professor of Biochemistry at the Faculty of Medicine and Surgery of Florence, coordinates the Cell Biology Laboratory of the Excellence and Research Center DENOThe?. Her studies on redox regulation of cell motility and cancer spreading, span from redox signalling during epithelial-mesenchymal transition, to the role of oxidative stress in the achievement of a metastatic and invasive phenotype. She contributed more than 100 original manuscripts and reviews in international peer-reviewed journals, dealing on motility, anchorage independence of cancer cells, achievement of anoikis resistance, epithelial mesenchymal transition or mesenchymal amoeboid transition and their regulation by tumor microenvironment.