Lactylation-dependent metabolic adaptation DOJINDO LABORATORIES

Previous Science Note

This article focusing on what type of posttranslational modification, lactilation, plays an important role in regulating cellular metabolism and may contribute to hepatocellular carcinoma progression. These findings may suggest the possibility that the functional effect of Lactilation not only in cancer cells but also the phenomena where metabolic shifts to glycolysis occur such as cellular senescence.

Lactylome analysis suggests lactylation-dependent mechanisms of metabolic adaptation in hepatocellular carcinoma
Zijian Yang, et. al., Nature Metabolism, 5, 61-79 (2023)

Point of Interest

- Lactate drives the posttranslational modification, lysine lactylation (Kla), on core histones but other targets remain unclear.

- Lactylome and proteome analysis of the tumors and adjacent livers reveals 99.8% of Kla sites are on non-histone proteins.

- Kla affects enzymes involved in metabolic pathways, including nucleotide metabolism.

- Lactylation at K28 inhibits adenylate kinase 2, facilitating the proliferation and metastasis of HCC cells.

Related Techniques

Glycolysis/Oxidative phosphorylation assay

Glycolysis/OXPHOS Assay Kit

Oxygen consumption rate assay

Extracellular OCR Plate Assay Kit

Glycolysis-related metabolites assay

Glucose and Lactate Assay Kit

TCA cycle-related metabolites assay

Glutamine, Glutamate, and α-KG Assay Kit

NAD(H) and NADP(H) redox couples assay

NAD/NADH and NADP/NADPH Assay Kit

ATP Assay

ATP Assay Kit

Nutrient uptake Assay

Glucose (Blue / Green / Red), Amino Acid, Cystine, and Fatty Acid Uptake Assay Kit

Lipid droplets detection

Lipi-Blue / Green / Red / Deep Red

Related Applications

Metabolic shift to glycolysis in senescenct cells

＜Evaluation by Lactate production and ATP levels＞

NAD(+) levels decline during the aging process, causing defects in nuclear and mitochondrial functions and resulting in many age-associated pathologies*. Here, we try to redemonstrate this phenomenon in the doxorubicin (DOX)-induced cellular senescence model with a comprehensive analysis of our products.

*S. Imai, et al., Trends Cell Biol, 2014, 24, 464-471