Research Paper Volume 12, Issue 16 pp 16255—16269
Glucose and cholesterol induce abnormal cell divisions via DAF-12 and MPK-1 in C. elegans
- 1 School of Nursing and Health, Henan University, Kaifeng 475004, Henan Province, China
- 2 School of Basic Medical Sciences, Henan University, Kaifeng 475004, Henan Province, China
- 3 Medical School, Henan University, Kaifeng 475004, Henan Province, China
Received: March 3, 2020 Accepted: June 19, 2020 Published: August 28, 2020https://doi.org/10.18632/aging.103647
How to Cite
Copyright © 2020 Qu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY) 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
People exposed to starvation have a high risk of developing cancer later in life, and prior studies have shown these individuals have high insulin and cholesterol levels and are sensitive to glucose. Using C. elegans as a model, we found that glucose and cholesterol can promote survival and cause starved L1 diapause worms to undergo abnormal neuronal cell divisions. Starvation has also been shown to promote long-term survival; however, we found that the functions of glucose and cholesterol in relation to these cell divisions are distinct from their effects on survival. We demonstrate that glucose functions in a DAF-16/FOXO-independent IIS pathway to activate the MAPK ontogenetic signaling to induce neuronal Q-cell divisions, and cholesterol works through DAF-12/steroidogenic pathways to promote these cell divisions. daf-12 and mpk-1/MAPK mutants suppress the function of glucose and cholesterol in these divisions, and a fully functioning dpMPK-1 requires the steroid hormone receptor DAF-12 for these divisions to occur. These afflictions also can be passed on to the immediate progeny. This work indicates a possible link between glucose and cholesterol in starved animals and an increased risk of cancer.