ArticleCancer & metabolism2021
Lipopolysaccharide promotes metastasis via acceleration of glycolysis by the nuclear factor-κB/snail/hexokinase3 signaling axis in colorectal cancer.
Article in Cancer & metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 51 citations in OpenAlex.
- Virulence factors of the microbiome: A functional toolkit for cancer progression (Review).Molecular and clinical oncology · 2026Review
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- Effects of FGF4/HIF-1α axis-mediated neuronal glycolysis on neuropathic pain.The journal of headache and pain · 2026Article
- Targeting Microbiome-Derived Exosomes to Overcome Cancer Therapy Resistance: Mechanisms, Implications, and Opportunities.Mini reviews in medicinal chemistry · 2026Review
- Gut microbial metabolites in colorectal cancer: dual roles in tumorigenesis, immune crosstalk, and therapeutic innovation.Frontiers in cellular and infection microbiology · 2026Review
- Molecular studies on the impact of microbiome on anticancer drug resistance.Frontiers in immunology · 2026Review
- The interplay of the microbiome and breast cancer: beyond the gut: a narrative review.Annals of medicine and surgery (2012) · 2025Review
- Targeting HK3 in tumor-associated macrophages enhances antitumor immunity through augmenting antigen cross-presentation in cervical cancer.Journal for immunotherapy of cancer · 2025Article
- Piperidine and valproic acid hybrid compound (F2S4-RSC advances · 2025Article
- Pharmacological Potential of Coriander Seeds: A Dual Action Agent Against LPS ofIndian journal of microbiology · 2025Article
- Rbfox3 Promotes Transformation of MDSC-Like Tumor Cells to Shape Immunosuppressive Microenvironment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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- Reliable hexokinase 3 protein detection in human cell lines and primary tissue.European journal of histochemistry : EJH · 2025Article
- Endotoxin-Free Outer Membrane Vesicles for Safe and Modular Anticancer Immunotherapy.ACS synthetic biology · 2025Article
- PreLect: Prevalence leveraged consistent feature selection decodes microbial signatures across cohorts.NPJ biofilms and microbiomes · 2025Article
- STsisal: a reference-free deconvolution pipeline for spatial transcriptomics data.Frontiers in genetics · 2025Article
- Beyond Tumor Borders: Intratumoral Microbiome Effects on Tumor Behavior and Therapeutic Responses.Immune network · 2024Review
- Role of glucose metabolic reprogramming in colorectal cancer progression and drug resistance.Translational oncology · 2024Review
- Dual inhibitory potential of ganoderic acid A on GLUT1/3: computational andRSC advances · 2024Article
- Sphinganine recruits TLR4 adaptors in macrophages and promotes inflammation in murine models of sepsis and melanoma.Nature communications · 2024Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundCancer cell is generally characterized by enhanced glycolysis. Inflammasome activation is interaction with glycolysis. The concentration of lipopolysaccharide (LPS), a classic inflammasome activator, is significantly higher in colorectal cancer tissue than in normal intestinal mucosa. However, the mechanism of LPS on glycolysis and metastasis has not been fully elucidated. This study aimed to investigate the roles of LPS on inflammasome activation, glycolysis, and metastasis, and unravel metformin's potential in treatment of CRC.
methodsWe detected inflammasome activation and cell motility following LPS exposure in CRC cell lines. Glycolysis analysis was performed, and the key glycolytic rate-limiting enzymes were detected. Dual-luciferase reporter gene assay, co-immunoprecipitation, chromatin immunoprecipitation (ChIP) analysis, and ChIP-reChIP assay were performed to identify the specific mechanisms of LPS on glycolysis. Mouse metastasis models were used to determine the effects of LPS and metformin on metastasis. Correlation analysis of the expression of various molecules was performed in 635 CRC samples from The Cancer Genome Atlas and 83 CRC samples from our lab.
resultsLPS activates caspase-1 through NF-κB and upregulates the expression of Snail and HK3 depending on caspase-1 activation. LPS potentiates migration and invasion depending on accelerated glycolysis, which could be reversed by knockdown of glycolytic rate-limiting enzyme HK3. Nuclear Snail is upregulated by NF-κB under LPS treatment and then forms a complex with NF-κB, then directly binds to the HK3 promoter region to upregulate the expression of HK3. Metformin suppresses the NF-κB/Snail/HK3 signaling axis that is activated by LPS and then inhibits LPS-induced metastasis. In vivo, LPS-treated cells form more metastasis in the lungs of mice, and metformin completely reverses this effect of LPS.
conclusionLPS activates inflammasomes in cancer cells through NF-κB and promotes metastasis through glycolysis enhanced by the NF-κB/Snail/HK3 signaling pathway in CRC. Metformin could prevent this effect of LPS.
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