Cancer Therapy Based on Oxidative Stress Modulation

Dear Colleagues,

Reactive oxygen species represent a group of highly reactive molecules involved as regulators of important signaling pathways. Moderate levels of ROS are required for several cellular functions, such as cell proliferation and differentiation. When the production of ROS increases or scavenged ROS decreases, cells undergo oxidative stress. Consequently, ROS can contribute to many pathological conditions, such as cancer. Several hall markers of tumor cells, such as cell transformation, genome instability, hyperproliferation, immortalization, angiogenesis, epithelial–mesenchymal transition, and metastasis are influenced in several ways by intracellular ROS. Moreover, many chemotherapeutic drugs and radiotherapy used in anticancer therapy induce oxidative stress. The induction of apoptosis (Type I programmed cell death) by elevated ROS levels was the main mechanism responsible for the positive effects of targeted cancer therapy based on monoclonal antibodies and tyrosine kinase inhibitors. Recently, a new therapeutic approach to kill cancer cells is based on autophagy (Type II programmed cell death) induced by ROS. Finally, increased ROS levels impair multidrug resistance of cancer cells mediated by ATP transporters, which causes cancer development and metastasis.

This Special Issue is based on the complex interconnection between ROS levels and cancer, essentially based on the balance between ROS production and scavenging. Its aim is to depict the development of anticancer therapy based on modulating intracellular ROS levels to treat cancer.

Dr. Maria Condello
Prof. Stefania Meschini
Guest Editor

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