Abstract:
Tumourigenic tissue uses modified metabolic signalling pathways in order to support
hyperproliferation and survival. Cancer-associated aerobic glycolysis resulting in lactic acid
production was described nearly 100 years ago. Furthermore, increased reactive oxygen
species (ROS) and lactate quantities increase metabolic, survival and proliferation
signalling, resulting in increased tumourigenesis. In order to maintain redox balance, the
cell possesses innate antioxidant defence systems such as superoxide dismutase, catalase
and glutathione. Several stimuli including cells deprived of nutrients or failure of
antioxidant systems result in oxidative stress and cell death induction. Among the cell
death machinery is autophagy, a compensatory mechanism whereby energy is produced
from damaged and/or redundant organelles and proteins, which prevents the
accumulation of waste products, thereby maintaining homeostasis. Furthermore,
autophagy is maintained by several pathways including phosphoinositol 3 kinases, the
mitogen-activated protein kinase family, hypoxia-inducible factor, avian myelocytomatosis
viral oncogene homolog and protein kinase receptor-like endoplasmic reticulum kinase.
The persistent potential of cancer metabolism, redox regulation and the crosstalk with
autophagy in scientific investigation pertains to its ability to uncover essential aspects of
tumourigenic transformation. This may result in clinical translational possibilities to exploit
tumourigenic oxidative status and autophagy to advance our capabilities to diagnose,
monitor and treat cancer.
