Emerging roles and the regulation of aerobic glycolysis in hepatocellular carcinoma

Jiao, Feng; Li, Jingjing; Wu, Liwei; Yu, Qiang; Ji, Jie; Wu, Jianye; Dai, Weiqi; Guo, Chuanyong

doi:10.1186/s13046-020-01629-4

Cited by 409 publications

(346 citation statements)

References 216 publications

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“…Although we found no differences in age, gender, T stage, N stage, AJCC stage, grade between glycolysis-H group and glycolysis-L group, the difference in M stage was obvious ( Table 1 ), which revealed that enhanced glycolytic activity facilitated invasion and metastasis in BLCA. This phenomenon was also revealed in pancreatic cancer [ 20 ], breast cancer [ 21 ], hepatocellular carcinoma [ 22 ], and gastric cancer [ 23 ].…”

Section: Resultsmentioning

confidence: 87%

Correlations between glycolysis with clinical traits and immune function in bladder urothelial carcinoma

Che

Han

et al. 2021

Bioscience Reports

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Background: Glycolysis was a representative hallmark in the tumor microenvironment, and we aimed to explore the correlations between glycolysis with immune activity and clinical traits in bladder urothelial carcinoma (BLCA). Method: Our study obtained glycolysis scores for each BLCA samples from TCGA by a single-sample gene-set enrichment analysis(ssGSEA) algorithm, based on a glycolytic gene set. The relationship between glycolysis with prognosis, clinical characteristics, and immune activity were investigated. Results: We found that enhanced glycolysis was associated with poor prognosis and metastasis in BLCA. Moreover, glycolysis had a close correlation with immune function, and enhanced glycolysis increased immune activities. In other words, glycolysis had a positive correlation with immune activities. Immune checkpoints such as IDO1, CD274, were up-regulated in high-glycolysis group as well. Conclusion: We speculated that in BLCA, elevated glycolysis enhanced immune function, which caused tumor cells to overexpress immune checkpoints to evade immune surveillance. Inhibition of glycolysis might be a promising assistant for immunotherapy in bladder cancer.

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Section: Resultsmentioning

confidence: 87%

Correlations between glycolysis with clinical traits and immune function in bladder urothelial carcinoma

Che

Han

et al. 2021

Bioscience Reports

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“…HK2 is a key enzyme associated with glycolysis, which contributes to multiple cell processes, like cell proliferation, invasion, migration, angiogenesis, and drug resistance in HCC. 36 Moreover, Huang et al showed that the up-regulation of HK2 increased glycolysis to promote cell migration and invasion in HCC. 37 Furthermore, multiple evidences suggested that HK2 could promote glycolysis and was responsible for migration and invasion in HCC.…”

Section: Discussionmentioning

confidence: 99%

NR2F1-AS1/miR-140/HK2 Axis Regulates Hypoxia-Induced Glycolysis and Migration in Hepatocellular Carcinoma

Li¹,

Li²,

Bai³

et al. 2021

CMAR

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“…The occurrence and progression of HCC are also closely intertwined with its metabolic disorders. Similar to most other solid tumors, the metabolic process of HCC cells has undergone many signi cant changes compared with normal liver cells, which are manifested in abnormally elevated glycolytic activity, increased de novo synthesis of fatty acids and decreased oxidation, as well as accelerated glutamine catabolism [2][3][4].…”

Section: Introductionmentioning

confidence: 99%

Glutamate dehydrogenase 1 mediated glutaminolysis sustains HCC cells proliferation and survival under glucose deprivation

Zhou¹,

Yu²,

Cheng³

et al. 2020

Preprint

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Background: It is generally believed that tumor cells could sustain its proliferation and survival under different nutrient status according to a so-called metabolic flexibility. How the metabolic flexibility of glutamine metabolism of HCC cells behaves under different glucose conditions has not yet been fully elucidated. In this study, we investigated how the glutamine metabolism modulate the proliferation and survival of HCC cells in response to different glucose conditions and explored the underlying molecular mechanism.Methods: Two cell lines SK-Hep-1 and PLC/PRF/5 were used to evaluate the glutamine addiction of HCC cells. Then, the cells were cultivated in high glucose medium (25mM glucose) and low glucose medium (1.0 mM glucose), respectively, to investigate whether glutaminolysis changed in response to different glucose levels. And, the underlying mechanism of glutamate dehydrogenase 1 (GDH1) sustaining HCC cells survival under glucose deprivation was explored. Additionally, the underlying correlation of GDH1 and glutamate–oxaloacetate transaminase 1 (GOT1) in glucose -poor HCC tissue was investigated.Results: HCC cells were addicted to glutamine. The glutaminolysis of HCC cells was different in response to different glucose conditions. That is, glutamate transaminases GOT1 involved glutamine metabolism played a dominant role in regulating cell growth when glucose was sufficient, while deaminase GDH1 mediated glutaminolysis became dominant when glucose was limited. Mechanically, low-glucose treated HCC cells could induce an elevated expression of GDH1 to supplement the TCA cycles in respond to glucose deprivation. Additionally, we further uncovered an underlying negative association between GDH1 and GOT1 in HCC tissues with decreased glucose levelsConclusions: GDH1 mediated pathway played a leading role in maintaining cell proliferation and survival under low glucose condition. By contrast, GOT1 mediated pathway was activated under high glucose condition. Mechanically, highly expressed GDH1 could drive the TCA cycle in response to glucose deprivation. Besides, there was a potential negative correlation between GDH1 and GOT1 in glucose-poor HCC tissues.

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Emerging roles and the regulation of aerobic glycolysis in hepatocellular carcinoma

Cited by 409 publications

References 216 publications

Correlations between glycolysis with clinical traits and immune function in bladder urothelial carcinoma

Correlations between glycolysis with clinical traits and immune function in bladder urothelial carcinoma

NR2F1-AS1/miR-140/HK2 Axis Regulates Hypoxia-Induced Glycolysis and Migration in Hepatocellular Carcinoma

Glutamate dehydrogenase 1 mediated glutaminolysis sustains HCC cells proliferation and survival under glucose deprivation

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