Scientists Uncover Cells’ Survival Strategy for Low-Nutrient Environments
A novel survival strategy may explain how cancer cells continue to adapt and grow, even when under metabolic stress.
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UCLA scientists have uncovered a surprising survival strategy in cells, especially cancer cells, that may help explain how they adapt and keep growing even when nutrients are scarce and under metabolic stress.
The team found that when cells are low on amino acids, which cells rely on to make proteins and grow, they activate a growth protein called MYC and alter the chromatin structure by reducing a specific chemical marker known as H4K20me1 that covers active genes. These two changes work in parallel to prime the cell’s capacity to produce proteins, enabling a rapid rebound in protein synthesis once nutrients become available. This unexpected increase in protein-making potential under nutrient-poor conditions may help explain how MYC-driven cancers survive and grow despite limited resources.
Background
The MYC gene, which is frequently activated in many cancers including hematological malignancies, colorectal, lung, stomach and various subtypes of breast cancer, plays a key role in boosting protein production. However, the epigenetic mechanisms that work alongside MYC to support this process, especially during amino acid shortages, have previously remained unclear.
Method
Scientists grew human cells with and without amino acids to study how DNA packaging and gene activity change during nutrient shortage. They used a combination of molecular tools to measure gene expression and protein production.
Impact
These findings open new avenues for targeting cancer metabolism and growth by revealing how cells use a chromatin-based strategy to remain primed for protein production, even under nutrient-poor conditions. Understanding how MYC helps cells survive and recover from nutrient stress could lead to new treatment strategies for targeting MYC-driven cancers and other diseases linked to metabolic stress.
“We discovered that during amino acid scarcity, cells don’t just shut down—they rewire themselves to be ready for a burst of protein synthesis once conditions improve,” said Dr. Siavash Kurdistani, professor and chair of biological chemistry at the David Geffen School of Medicine at UCLA, investigator at the UCLA Health Jonsson Comprehensive Cancer Center and senior author of the study. “Understanding this priming mechanism could open new paths for targeting how cancer cells adapt and survive under stress.”
Reference: Cheng C, Su T, Morselli M, Kurdistani SK. Coordinated histone methylation loss and MYC activation promote translational capacity under amino acid restriction. Cancer Metab. 2025;13(1):29. doi: 10.1186/s40170-025-00399-x
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