Mitochondrial Function and Dysfunction in Cancer and Their Potential as Anti-cancer Targets (Volume II)

Dear Colleagues,

This collection is the second edition of the previous one, "Mitochondrial function and dysfunction in cancer and their potential as anti-cancer targets" (https://www.mdpi.com/journal/cancers/special_issues/mfdctpaat).

The mitochondrion, a discrete sub-cellular organelle comprising some 1000 different proteins, mediates basic life functions and contains key components of biosynthetic pathways. It also serves as the site where cellular decisions leading to apoptosis (programmed cell death) are taken. Mitochondria perform a variety of crucial cell functions, including energy production; Ca²⁺ signaling and the maintenance of Ca²⁺ homeostasis; the metabolism of amino acids, lipids, and iron; modulation of the cell’s redox potential; osmotic regulation and pH control; in addition to being the site of reactive oxygen species (ROS) generation and an essential component of the apoptotic machinery. Changes in these parameters can impact biosynthetic pathways, cellular signal transduction pathways, and epigenetics, shifting the cell from the quiescent, differentiated state to one of active proliferation, as occurs in cancer. Indeed, the signaling pathways that govern mitochondrial function, mitochondrial integrity, cell viability and apoptosis have been addressed in many studies, with mitochondrial targeting strategies having recently gained momentum.

The association of mitochondria with cancer was first presented over 70 years ago by Otto Heinrich Warburg and his colleagues, who hypothesized that dysfunctional mitochondria may be the cause of higher rates of aerobic glycolysis (termed the “Warburg effect”), with this gradual and cumulative decrease in mitochondrial activity being associated with malignant transformation. However, many studies conducted since have demonstrated that functional mitochondria are essential for the cancer cell and have identified pleiotropic roles of mitochondria in tumorigenesis.

Given their multifunctionality it is not surprising that mitochondria are important mediators of tumorigenesis—a process requiring flexibility in adapting to cellular and environmental alterations. Thus, uncovering the mechanisms responsible for altered mitochondrial function during tumorigenesis is critical for developing the next generation of cancer therapeutics. Indeed, appreciation that mitochondria play central roles in cellular energy generation, metabolism, apoptosis and necrosis carry far-reaching implications and provide solid rationale and a strong biological basis for developing mitochondria-targeted anti-cancer agents.

Scientists studying mitochondria- and cancer-associated topics, including but not limited to oxidative stress, organelle biogenesis, apoptosis, necrosis, import and folding of mitochondrial proteins, membrane synthesis, structure and dynamics, Ca²⁺ homeostasis, the mitochondrial genetic system, mitochondria-interacting proteins (e.g., hexokinase, anti- and pro-apoptotic proteins, p53), as well as ER–mitochondria interactions and cancer, are invited to contribute to this Special Issue.

Prof. Dr. Varda Shoshan-Barmatz
Dr. Manikandan Santhanam
Guest Editors

Manuscript Submission Information

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• apoptosis
• mitochondria
• metabolism
• cancer
• tumor microenvironment
• apoptogenic proteins
• oxidative stress
• mitochondrial DNA
• Ca²⁺ signaling