Transcriptional regulation and post-translational modifications in the glycolytic pathway for targeted cancer therapy

Ni, Xuan; Lu, Cheng-piao; Xu, Guo-qiang; Ma, Jing-jing

doi:10.1038/s41401-024-01264-1

Cited by 7 publications

(1 citation statement)

References 272 publications

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“…The Warburg effect posits that cancer cells undergo a metabolic shift, prioritizing glycolysis over oxidative phosphorylation for energy production [ 82 ]. Despite glycolysis being less efficient than oxidative phosphorylation in terms of ATP production per glucose molecule, cancer cells benefit from the higher rate of ATP production through glycolysis ( Figure 3 A).…”

Section: Metabolic Shifts and Reprogramming In Masld-induced Hccmentioning

confidence: 99%

Crosstalk between Epigenetics and Metabolic Reprogramming in Metabolic Dysfunction-Associated Steatotic Liver Disease-Induced Hepatocellular Carcinoma: A New Sight

Li,

Wang,

Zhao

et al. 2024

Metabolites

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Epigenetic and metabolic reprogramming alterations are two important features of tumors, and their reversible, spatial, and temporal regulation is a distinctive hallmark of carcinogenesis. Epigenetics, which focuses on gene regulatory mechanisms beyond the DNA sequence, is a new entry point for tumor therapy. Moreover, metabolic reprogramming drives hepatocellular carcinoma (HCC) initiation and progression, highlighting the significance of metabolism in this disease. Exploring the inter-regulatory relationship between tumor metabolic reprogramming and epigenetic modification has become one of the hot directions in current tumor metabolism research. As viral etiologies have given way to metabolic dysfunction-associated steatotic liver disease (MASLD)-induced HCC, it is urgent that complex molecular pathways linking them and hepatocarcinogenesis be explored. However, how aberrant crosstalk between epigenetic modifications and metabolic reprogramming affects MASLD-induced HCC lacks comprehensive understanding. A better understanding of their linkages is necessary and urgent to improve HCC treatment strategies. For this reason, this review examines the interwoven landscape of molecular carcinogenesis in the context of MASLD-induced HCC, focusing on mechanisms regulating aberrant epigenetic alterations and metabolic reprogramming in the development of MASLD-induced HCC and interactions between them while also updating the current advances in metabolism and epigenetic modification-based therapeutic drugs in HCC.

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Section: Metabolic Shifts and Reprogramming In Masld-induced Hccmentioning

confidence: 99%