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Metabolic state determines drug response in liver cancer

ABSTRACT: Metabolic state determines drug response in liver cancer

PROVIDER: PRJNA507425 | ENA |

REPOSITORIES: ENA

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Metabolic state determines drug response in liver cancer

Project description:Drug resistance is one of the most challenging problems in liver cancer research. The hepatocellular carcinoma cell line HLE is highly dependent on exogenous glutamine for proliferation. In this cell line, we have found that glutamine deprivation leads to proliferation arrest, phosphorylation of extracellular signal-regulated kinase (ERK), and metabolic alterations at gene, protein, metabolite levels. Interestingly, while HLE cells respond to kinase inhibitors in their unperturbed metabolic state, they display pro-tumourigenic phenotypes such as increased aerobic glycolysis and proliferation when treated with inhibitors of MAPK/ERK pathway in the impaired metabolic state induced by glutamine deprivation. Thus, the aim of this microarray analysis is to determine the genomic alterations that accompany glutamine deprivation and treatment with pERK inhibitor U0126. The anticipated alterations could shed light on novel molecular mechanisms underlying drug resistance, and may be useful for predicting therapeutic response in liver cancer.

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Project description:Paracetamol (acetaminophen, APAP) overdose severely damages mitochondria and triggers several apoptotic processes in hepatocytes, but the final outcome is fulminant necrotic cell death, resulting in acute liver failure and mortality. Here, we studied this switch of cell death modes and demonstrate a non-canonical role of the apoptosis-regulating BCL-2 homolog BIM/Bcl2l11 in promoting necrosis by regulating cellular bioenergetics. BIM deficiency enhanced total ATP production and shifted the bioenergetic profile towards glycolysis, resulting in persistent protection from APAP-induced liver injury. Modulation of glucose levels and deletion of mitofusins confirmed that severe APAP toxicity occurs only in cells dependent on oxidative phosphorylation. Glycolytic hepatocytes maintained elevated ATP levels and reduced ROS, which enabled lysosomal recycling of damaged mitochondria by mitophagy. The present study highlights how metabolism and bioenergetics affect drug-induced liver toxicity, and identifies BIM as important regulator of glycolysis, mitochondrial respiration, and oxidative stress signaling.

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Drug-Induced Liver Injury (DILIN) GWAS

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