Cancer Prevention and Therapy by Targeting Oxidative Stress Pathways
A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Medicinal Chemistry".
Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 496
Special Issue Editors
Interests: pharmacology; therapeutic modulators of oxidative stress
Special Issues, Collections and Topics in MDPI journals
Interests: neurodegeneration; inflammation; cell death mechanisms; anticancer compounds; targeted therapy
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
As cancer research continues at a rapid pace, it is of great importance to identify new molecular targets. Several pathways including the autophagy, inflammation, and deficiency of apoptotic and ferroptotic signaling pathways are involved in the initiation and development of cancer. Additionally, increased DNA mutations, DNA damage, genome instability, and ultimately cell proliferation induced by oxidative stress have been linked to cancer progression. Although oxidative stress is mainly associated with cellular damage, excess free radicals are known to promote tumor cell proliferation, angiogenesis, and metastasis in a wide variety of cancers. Thus, targeting oxidative stress is a good strategy to explore new, safe, and more effective treatments for cancer prevention and therapy.
The cross-talk between cancer and oxidative stress signaling is based on the synchronization between reactive oxygen species (ROS) generation and clearance for the maintenance of redox homeostasis. Intracellular ROS is a hallmark in cancer that plays a key role in cell survival, proliferation, epithelial–mesenchymal transition, and metastasis as well as in the necrosis, apoptosis, and autophagy of tumor cells. Cancer cells have naturally increased ROS levels due to their high energy demand. In view of this, different approaches to ROS-related anticancer therapies have been considered. In one approach, scavenging intracellular ROS using antioxidants increases cell death in cancer cells by depriving energy production in the early stages of tumorigenesis. Another approach is based on increasing ROS generation over the cytotoxic threshold and can selectively kill cancer cells by stimulating redox-dependent cell death through the apoptosis, necrosis, autophagy, and ferroptosis pathways.
Another potential target for anticancer therapy is the ROS-induced autophagy that depends on the developmental stage of the tumor. Due to the strong connection between these two cellular mechanisms during the course of cancer initiation and progression, the use of autophagy modulators could be a potential new of cancer treatment.
Another potential approach could be switching oxidative stress-targeted proteins in order to create new possibilities for cancer treatment via cancer redox signaling. In this context, Nrf2 is a key driver in cellular defence against oxidative stress and cellular survival. Therefore, the role of Nrf2-targeted drugs in different types of cancer is of great relevance in terms of therapeutic interventions to promote the fabrication of new chemotherapeutic agents in the future.
Potential topics include, but are not limited to:
- Advances in redox-active prodrugs in cancer;
- Natural or synthetic small molecules as ROS-targeted anticancer therapeutics;
- Non-radical scavenging mechanisms targeting oxidative stress in cancer;
- Nrf2/Keap1 pathway-targeted therapeutics in cancer;
- Preclinical designing and development of small molecules targeting redox regulation for their cancer therapeutic potential;
- Clinical studies on redox therapies as anticancer agents;
- Biomarkers for assessing redox imbalance and antioxidant status;
- Imaging technologies for oxidative stress in cancer.
Prof. Dr. Luciano Saso
Dr. Guliz Armagan
Dr. Sarmistha Saha
Guest Editors
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Keywords
- redox signaling
- reactive oxygen species
- cancer therapy
- cell signaling
- apoptosis
- autophagy
- Nrf2
