Redox State, Mitochondrial Metabolism and Autophagy in Cancer and Its Modulation by Antitumor Agents and Immunotherapy

Dear Colleagues,

Several antitumoral treatments exert their function through changes in the redox state, mitochondrial metabolism, and autophagy process of the tumoral cells. Meanwhile, some types of cancer require certain reactive oxygen species (ROS) levels to grow and develop metastasis; other types of cancer need reduced ROS levels to induce metastasis. It should be noted that high ROS levels also induce cell death as ROS can overcome the cell tumor umbral of resistance to oxidative stress (OS). Thus, cancer progression may depend on ROS, but ROS overproduction could be a therapeutic target to induce cancer cell death. Moreover, OS can induce mitochondrial damage and its dysfunction and, consequently, cell death. Autophagy is a degradation process that can degrade these dysfunctional mitochondria to promote new mitochondria biogenesis; if this cellular mechanism is not functioning properly, the tumor decreases because of the accumulation of damaged organelles. Thus, redox state, mitochondrial dysfunction, and autophagy are key events for cancer and metastasis reduction, and the exploration of these processes is crucial for the induction of metastasis and cancer reduction. Moreover, the immune response of the cancer patient associated with the latter processes plays a fundamental role in cancer elimination. Reviews and original research manuscripts that explore the effects of ROS, OS, autophagy, and immune response related to cancer development and its elimination, including antitumor agents and immunotherapy, are welcome to this Special Issue.

Prof. Dr. José Pedraza Chaverri
Guest Editor

Dr. Alfredo Cruz-Gregorio
Guest Editor Assistant

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