Guest Editors
Dr. Tasleem Arif, Department of Cell, Developmental & Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, USA. tasleem.arif@mssm.edu
Summary
Cancer is a complicated disease with several genetic, epigenomic,
transcriptomic, proteomic, and metabolic abnormalities. Otto Warburg described
the altered metabolism of cancer cells in 1924, demonstrating that they
anaerobically consume glucose, followed by an increase in lactate production.
Lactate promotes the survival and growth of cancer cells in the tumor
microenvironment. Cancer cells' altered metabolism is recognized as a critical
characteristic of cancer since it regulates cancer growth and invasion-related
activities. Metabolic reprogramming is required for cancer cell survival in
hypoxia, for immune monitoring of cancer cells, and for fast cell
multiplication, which enhances tumor cells' biological activity.
Notably, cancer cell plasticity necessitates frequent changes in
cellular metabolism and immune system activation to maintain a balance between
tumor development and expansion. While it is well established that this confers
growth benefits on the tumor, the intracellular interplay underlying these
alterations remains unknown. The mitochondria are critical regulators of this
process.
Mitochondria are organelles that are involved in bioenergy production,
biosynthesis, and signaling. Mitochondrial signaling is critical for recognizing
and responding to cellular stress. As a result, mitochondrial function and
signaling are thought to be important modulators of carcinogenesis and cancer
therapy. Additionally, they are crucial to immunity. Indeed, mitochondria may
serve as a platform for the activation of innate immunity signaling through the
mitochondrial antiviral–signaling protein (MAVS) located on their outer
membrane. Simultaneously, since mitochondria are the primary source of reactive
oxygen species (ROS), mitochondrial DNA (mtDNA) is continually subjected to
oxidative stress, which results in a steady buildup of detrimental mutations if
not addressed. This eventually results in mitochondrial malfunction and the
release of mtDNA into the cytosol, where it behaves as a danger-associated
molecular pattern (DAMP), activating important innate immune signaling pathways
such as TLR9 and cGAS/STING. Mitochondrial metabolic inefficiency caused by
mtDNA mutations has been reported in a variety of malignancies and is strongly
linked with a poor prognosis in patients.
This Special Issue will cover a variety of topics related to
next-generation cancer therapies and the mitochondrial function pathway in
cancer formation and progression. A better knowledge of mitochondrial metabolic
dysfunction and signaling will shed light on a critical aspect of tumor cell
biology and may possibly uncover potential therapeutic targets.
Keywords
Mitochondria, Cancer Cell, Metabolism, Signaling, Mtdna, ROS, Mitochondrial Dysfunction, Metabolic Pathways, Inflammation, Therapy Targets
Published Papers
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