Academia Sinica researchers said they have identified a key protein in regulating the self-eating process of cells — a recycling mechanism of the body to disassemble unnecessary or defective cellular components — adding that the findings could further the understanding of diseases related to dysfunctions of the process, such as cancer, neurodegeneration and muscle atrophy.
Academia Sinica research fellow Chen Ruey-hwa (陳瑞華) told a news conference yesterday that her team discovered a protein, Kelch-like protein 20 (KLHL20), which could control the termination of a cell’s self-eating process, or autophagy, by forming an enzyme complex that can catalyze the degradation of multiple autophagy-initiating factors at the onset of autophagy.
The KLHL20-based enzyme complex degrades other autophagy proteins by inducing hydrolysis — the breaking of a chemical bond in a molecule using water — in those proteins, and the degradation events collectively lead to the termination of the process, Chen said.
During autophagy, cellular components are delivered from the cell cytoplasm for degradation and recycling, which is important, as it removes harmful substances such as damaged organelles and infectious agents to maintain cellular stability in response to various stressed conditions, Chen said, adding that failure to terminate autophagy promotes cell death and muscle atrophy.
Past research has been focused on how autophagy occurs, and it remains unknown how the autophagy process is turned off once it is induced, Chen said.
In tests, the team removed KLHL20 from mice with diabetes, which caused the animals to experience more severe muscle atrophy compared with diabetic mice with KLHL20, indicating the protein has a key role in terminating autophagy to maintain cell survival and tissue homeostasis.
Excessive autophagy leads to unrestrained cellular degradation, which can result in muscle atrophy and diabetes, and can also promote the survival of harmful cells, such as cancerous cells, she said.
Insufficient autophagy leads to the accumulation of harmful substances in the body, which can cause neurodegenerative conditions such as Alzheimer’s disease and spinocerebellar atrophy, she said.
“Both excessive and insufficient autophagy can lead to certain diseases, but we might be able to regulate autophagy by regulating KLHL20. However, we have yet to understand how to speed up and slow down autophagy, which is to be the focus of future experiments,” she said, adding that new therapies could be developed with a KLHL20 inhibitor or promoter.
The results of the team’s research were published in the academic journal Molecular Cell earlier this month.
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