Liver tumors may depend on LARS to withstand stress and keep multiplying

by Jonathan King, University of Illinois at Urbana-Champaign

edited by Alexander Pol

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Illinois researchers made a breakthrough discovery in the fight against liver cancer. Collaborators Lin-Feng Chen, Susan A. Martinis, and graduate student Xiaodan Lin found that decreasing protein levels of leucyl-tRNA synthetase (LARS) impedes liver cancer cell multiplication.

Liver cancer is highly challenging to treat because of difficulties in early diagnosis and its high recurrence rate. It remains one of the top causes of cancer-related mortality worldwide and is the second-leading cause of cancer-related death after lung cancer. The research team noted that LARS is highly expressed in liver tumors and associated with poor patient survival, making LARS a promising therapeutic target for liver cancer.

"LARS helps liver cancer cells stay metabolically fit and continue growing," said Cancer Center at Illinois (CCIL) member Chen. "When LARS levels are lowered, cancer cells experience mitochondrial stress, accumulate damaging reactive oxygen species, activate autophagy and, ultimately, enter a senescent state where they stop proliferating."

How did the team identify LARS as a focus of their study?

"LARS has long been known as a housekeeping enzyme that is essential for cells to make proteins by attaching the amino acid leucine to its corresponding tRNA to translate the genetic code," said Martinis. "However, LARS 'moonlights' with additional functions: For example, it can act as a nutrient sensor that activates growth-promoting pathways such as mTORC1 in response to leucine availability. Elevated LARS expression has also been reported in certain cancers—including lung cancer and osteosarcoma—suggesting it may have cancer-promoting functions beyond protein synthesis."

Because LARS is both a protein-making enzyme and a nutrient sensor, Chen, Martinis and Lin wanted to determine whether liver cancer cells depend on it.

"Our study sought to answer whether disrupting LARS levels could expose a weakness in liver cancer cells and provide a new avenue for therapy," added Chen.

To perform this analysis, Lin relied on HepG2 liver cells and expected that removing LARS from the HepG2 cells would slow cancer cell growth by shutting down protein production. "Surprisingly, protein production remained largely intact," Martinis shared. "Rather, the cancer cells became stressed, their mitochondria became dysfunctional, they aged prematurely and stopped dividing. This revealed an unexpected, influential role for LARS in helping cancer cells stay healthy and continue growing."

Chen, Martinis and Lin discovered liver cancer cells' reliance on LARS to cope with stress and continue growing.

This basic science discovery lays a foundation for future translational work, which could lead to new targeted treatments and help doctors identify patients with more aggressive cancers who may benefit from personalized therapies. Chen and Martinis aim to understand the mechanistic details of how LARS contributes to liver cancer cell survival as a next step in their partnership in identifying a new treatment strategy.

More information

Xiaodan Lin et al, LARS regulates cellular senescence and autophagy in liver cancer cells, Cell Death & Disease (2026). DOI: 10.1038/s41419-026-09114-0

Key medical concepts

Liver CancerLiver NeoplasmsAutophagy

Clinical categories

OncologyGastroenterology Provided by University of Illinois at Urbana-Champaign Who's behind this story?

Alexander Pol

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