Abstract
Alterations from the normal set of chromosomes are extremely common as cells progress toward tumourigenesis. Similarly, we expect to see disruption of normal cellular metabolism, particularly in the use of glucose. In this review, we discuss the connections between these two processes: how chromosomal aberrations lead to metabolic disruption, and vice versa. Both processes typically result in the production of elevated levels of reactive oxygen species, so we particularly focus on their role in mediating oncogenic changes.
Highlights
Aneuploidy, an abnormal set of chromosomes, was first identified as a biomarker for epithelial cancer in the late 1800s [1], and remains a typical feature of advanced cancers, with more than 80% of solid tumours showing visible chromosomal abnormalities [2]
Glycolysis is critical for providing biosynthetic precursors for nucleotide and amino acid synthesis that are rate limiting for proliferation
It appears that aneuploid cells use reactive oxygen species (ROS) to enhance relatively minor alterations in ploidy into a significant damage signal that disrupts protein folding and DNA homeostasis, as well as mitochondrial metabolism levels could contribute to the formation of protein aggregates, putting more stress on the endoplasmic reticulum (ER), which results in more ROS, creating a feedback loop that should result in the death of defective cells
Summary
Aneuploidy, an abnormal set of chromosomes, was first identified as a biomarker for epithelial cancer in the late 1800s [1], and remains a typical feature of advanced cancers, with more than 80% of solid tumours showing visible chromosomal abnormalities [2]. It has been known for many decades that tumours typically show altered patterns of energy use, an elevated rate of glycolysis [3]. We examine the connections between aneuploidy and metabolism in driving tumorigenesis, with a particular focus on the role of oxidative stress
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have