AI Article Synopsis
- Cancer cells reprogram their metabolism, and a specific type of protein modification called malonylation is linked to this process and cancer growth, though its role is not fully understood.
- Research on hepatocellular carcinoma (HCC) showed reduced levels of malonyl-CoA and a general decline in protein malonylation, but increased malonylation of the protein nucleolin (NCL) was found in HCC samples.
- NCL's malonylation encourages its movement in the cell, allowing it to bind to AKT mRNA and enhance AKT production, which is crucial for HCC cell proliferation; reducing AKT levels effectively slowed down the growth of these cancer cells.
Article Abstract
Cancer cells undergo metabolic reprogramming that is intricately linked to malignancy. Protein acylations are especially responsive to metabolic changes, influencing signal transduction pathways and fostering cell proliferation. However, as a novel type of acylations, the involvement of malonylation in cancer remains poorly understood. In this study, we observed a significant reduction in malonyl-CoA levels in hepatocellular carcinoma (HCC), which correlated with a global decrease in malonylation. Subsequent nuclear malonylome analysis unveiled nucleolin (NCL) malonylation, which was notably enhanced in HCC biopsies. we demonstrated that NCL undergoes malonylation at lysine residues 124 and 398. This modification triggers the translocation of NCL from the nucleolus to nucleoplasm and cytoplasm, binding to AKT mRNA, and promoting AKT translation in HCC. Silencing AKT expression markedly attenuated HCC cell proliferation driven by NCL malonylation. These findings collectively highlight nuclear signaling in modulating AKT expression, suggesting NCL malonylation as a novel mechanism through which cancer cells drive cell proliferation.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11525140 | PMC |
| http://dx.doi.org/10.1016/j.jbc.2024.107785 | DOI Listing |
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