Targeting hepatocellular carcinoma growth and metabolism: A synergistic approach with para-toluenesulfonamide and radiofrequency ablation

Liu, Na; Zhang, Jianzeng; Wu, Jiaojiao; Feng, Fan; Chai, Yantao; Li, Yongwu; Liu, Bo

doi:10.1016/j.iliver.2024.100111

iLIVER

2024

DOI: 10.1016/j.iliver.2024.100111

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Targeting hepatocellular carcinoma growth and metabolism: A synergistic approach with para-toluenesulfonamide and radiofrequency ablation

Na Liu,

Jianzeng Zhang,

Jiaojiao Wu

et al.

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2024

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Pralatrexate represses the resistance of HCC cells to molecular targeted agents via the miRNA-34a/Notch pathway

Jin,

Liu,

Sun

et al. 2024

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Metabolism-related pathways are important targets for intervention in the treatment of hepatocellular carcinoma (HCC), but few studies have reported on the combination of inhibitors of folate metabolism-related enzymes and molecularly targeted drugs for HCC. The results of the present work are the first to reveal the effects of an inhibitor of dihydrofolate reductase (DHFR), pralatrexate, on the sensitivity of HCC cells to molecularly targeted agents examined using multiple assays. In HCC cells, knockdown of DHFR or treatment with pralatrexate enhanced the sensitivity of HCC cells to molecularly targeted agents, such as sorafenib, regorafenib, lenvatinib, cabozantinib, or anlotinib. Mechanically, pralatrexate decreased the methylation rates of miRNA-34a’s promoter region to enhance the expression of miRNA-34a. Treatment with pralatrexate inhibited the expression of Notch and its downstream factors by enhancing the expression of miRNA-34a in HCC cells. In clinical specimens, the expression of miRNA-34a was negatively correlated with DHFR expression, while DHFR expression was positively correlated with the Notch intracellular domain (NICD) and downstream factors of the Notch pathway. The expression of miRNA-34a was negatively correlated with DHFR expression, while the methylation rates of miRNA-34a’s promoter were positively related to DHFR. The effect of pralatrexate on the metabolic profile of HCC cells is very different from that of small molecule inhibitors related to glycolipid metabolism. Therefore, pralatrexate upregulates the sensitivity of HCC cells to molecularly targeted drugs. These results expand our understanding of folate metabolism and HCC and can help provide more options for HCC treatment. Supplementary Information The online version contains supplementary material available at 10.1007/s12672-024-01572-2.

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Pralatrexate represses the resistance of HCC cells to molecular targeted agents via the miRNA-34a/Notch pathway

Jin,

Liu,

Sun

et al. 2024

Discov Onc

View full text Add to dashboard Cite

show abstract

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Targeting hepatocellular carcinoma growth and metabolism: A synergistic approach with para-toluenesulfonamide and radiofrequency ablation

Cited by 1 publication

References 54 publications

Pralatrexate represses the resistance of HCC cells to molecular targeted agents via the miRNA-34a/Notch pathway

Pralatrexate represses the resistance of HCC cells to molecular targeted agents via the miRNA-34a/Notch pathway

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