Advanced progress of spatial metabolomics in head and neck cancer research

Zhao, Huiting; Shi, Chaowen; Han, Wei; Luo, Guanfa; Huang, Yumeng; Fu, Yujuan; Lu, Wen; Hu, Qingang; Shang, Zhengjun; Yang, Xihu

doi:10.1016/j.neo.2023.100958

Cited by 2 publications

(1 citation statement)

References 103 publications

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“…This highlights the metabolic alterations that cancer cells acquire in order to produce more ATP and metabolic intermediates, which power the synthesis of biological macromolecules and aid in cell survival, development, and multiplication. An acidic microenvironment is created by pyruvate, an end product of glycolysis that preferentially accumulates in cancer cells and is transformed to lactic acid by lactate dehydrogenase, which promotes the growth and invasion of cancer cells 10 , 11 . In HNSCC, there is an adverse correlation between high lactic acid levels and overall patient survival 12 .…”

Section: Introductionmentioning

confidence: 99%

Coenzyme Q₀ inhibited the NLRP3 inflammasome, metastasis/EMT, and Warburg effect by suppressing hypoxia-induced HIF-1α expression in HNSCC cells

Yang,

Chang,

Vadivalagan

et al. 2024

Int. J. Biol. Sci.

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Coenzyme Q0 (CoQ0), a quinone derivative from Antrodia camphorata, has antitumor capabilities. This study investigated the antitumor effect of noncytotoxic CoQ0, which included NLRP3 inflammasome inhibition, anti-EMT/metastasis, and metabolic reprogramming via HIF-1α inhibition, in HNSCC cells under normoxia and hypoxia. CoQ0 suppressed hypoxia-induced ROS-mediated HIF-1α expression in OECM-1 and SAS cells. Under normoxia and hypoxia, the inflammatory NLRP3, ASC/caspase-1, NFκB, and IL-1β expression was reduced by CoQ0. CoQ0 reduced migration/invasion by enhancing epithelial marker E-cadherin and suppressing mesenchymal markers Twist, N-cadherin, Snail, and MMP-9, and MMP-2 expression. CoQ0 inhibited glucose uptake, lactate accumulation, GLUT1 levels, and HIF-1α−target gene (HK-2, PFK-1, and LDH-A) expressions that are involved in aerobic glycolysis. Notably, CoQ0 reduced ECAR as well as glycolysis, glycolytic capability, and glycolytic reserve and enhanced OCR, basal respiration, ATP generation, maximal respiration, and spare capacity in OECM-1 cells. Metabolomic analysis using LC-ESI-MS showed that CoQ0 treatment decreased the levels of glycolytic intermediates, including lactate, 2/3-phosphoglycerate, fructose 1,6-bisphosphate, and phosphoenolpyruvate, and increased the levels of TCA cycle metabolites, including citrate, isocitrate, and succinate. HIF-1α silencing reversed CoQ0-mediated anti-metastasis (N-Cadherin, Snail, and MMP-9) and metabolic reprogramming (GLUT1, HK-2, and PKM-2) under hypoxia. CoQ0 prevents cancer stem-like characteristics (upregulated CD24 expression and downregulated CD44, ALDH1, and OCT4) under normoxia and/or hypoxia. Further, in IL-6-treated SG cells, CoQ0 attenuated fibrosis by inhibiting TGF-β and Collagen I expression and suppressed EMT by downregulating Slug and upregulating E-cadherin expression. Interesting, CoQ0 inhibited the growth of OECM-1 tumors in xenografted mice. Our results advocate CoQ0 for the therapeutic application against HNSCC.

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Section: Introductionmentioning

confidence: 99%

Coenzyme Q₀ inhibited the NLRP3 inflammasome, metastasis/EMT, and Warburg effect by suppressing hypoxia-induced HIF-1α expression in HNSCC cells

Yang,

Chang,

Vadivalagan

et al. 2024

Int. J. Biol. Sci.

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Multi-omics study on the molecular mechanism of anlotinib in regulating tumor metabolism

Lu,

Han,

Zhang

et al. 2024

European Journal of Pharmacology

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Advanced progress of spatial metabolomics in head and neck cancer research

Cited by 2 publications

References 103 publications

Coenzyme Q₀ inhibited the NLRP3 inflammasome, metastasis/EMT, and Warburg effect by suppressing hypoxia-induced HIF-1α expression in HNSCC cells

Coenzyme Q₀ inhibited the NLRP3 inflammasome, metastasis/EMT, and Warburg effect by suppressing hypoxia-induced HIF-1α expression in HNSCC cells

Multi-omics study on the molecular mechanism of anlotinib in regulating tumor metabolism

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Advanced progress of spatial metabolomics in head and neck cancer research

Cited by 2 publications

References 103 publications

Coenzyme Q0 inhibited the NLRP3 inflammasome, metastasis/EMT, and Warburg effect by suppressing hypoxia-induced HIF-1α expression in HNSCC cells

Coenzyme Q0 inhibited the NLRP3 inflammasome, metastasis/EMT, and Warburg effect by suppressing hypoxia-induced HIF-1α expression in HNSCC cells

Multi-omics study on the molecular mechanism of anlotinib in regulating tumor metabolism

Contact Info

Product

Resources

About

Coenzyme Q₀ inhibited the NLRP3 inflammasome, metastasis/EMT, and Warburg effect by suppressing hypoxia-induced HIF-1α expression in HNSCC cells

Coenzyme Q₀ inhibited the NLRP3 inflammasome, metastasis/EMT, and Warburg effect by suppressing hypoxia-induced HIF-1α expression in HNSCC cells