Fusobacterium periodonticum BCT Protein Targeting Glucose Metabolism to Promote the Epithelial-mesenchymal Transition of Esophageal Cancer Cells by Lactic Acid

Q: What role does BCT from Fusobacterium periodonticum play in esophageal cancer cells?

BCT shows higher expression in esophageal cancer tumor tissues and enhances survival, invasion, and migration of esophageal cancer cells.

Q: How does BCT alter glucose metabolism and lactate production?

BCT augments hypotaurine metabolism and glycolysis/gluconeogenesis, leading to decreased glucose and pyruvate while increasing LDH activity and lactic acid.

Q: Which signaling pathways link BCT and lactic acid to EMT and metastasis?

BCT upregulates TLR4, Akt, and HIF-1α, which regulate lactic acid production; lactic acid then increases GPR81, Wnt, and β-catenin to induce EMT and metastasis.

Sep 22, 2026

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Cancer microbiota is linked to tumor progression, with Fusobacterium periodonticum found at higher abundance in esophageal cancer tissues. Bioinformatics indicated BCT as a key virulence protein, motivating investigation of its mechanism in esophageal cancer. Eukaryotic expression and recombinant BCT were used alongside CCK8, UPLC-MS/MS, ELISA, transwell assays, RT-qPCR, and WB to connect BCT to glycolysis, lactate production, EMT, and metastasis via TLR4/Akt/HIF-1α and GPR81/Wnt/β-catenin signaling.

LanguageEnglish

CategoryResearch & Report

FormatPDF

Pages15

Reading Time38 min

AccessFree to download

Abstract

Background

Methods

Results

Conclusion

Introduction

Esophageal cancer burden and current treatments

Guo et al. Journal of Translational Medicine (2024) 22:401 [https://doi.org/10.1186/s12967-024-05157-z](https://doi.org/10.1186/s12967-024-05157-z) Journal of Translational Medicine RESEARCH Open Access Fusobacterium periodonticum BCT protein targeting glucose metabolism to promote the epithelial-mesenchymal transition of esophageal cancer cells by lactic acid Xinxin Guo 1, Ping Wan 1, Weitao Shen 1, Mingjun Sun 1, Zhenyan Peng 1, Yinghao Liao 1, Yang Huang 1 and Ran Liu 1* Abstract Background The cancer microbiota was considered the main risk factor for cancer progression. We had proved that Fusobacterium periodonticum (F. p) was higher abundance in Esophageal cancer(EC)tissues. Bioinformation analysis found that BCT was a key virulence protein of F. p. However, little is known about the role and mechanism of BCT in EC. This study aimed to recognize the key virulence protein of F. p and explore the mechanism of BCT in promoting EC. Methods We constructed a eukaryotic expression vector and purified the recombinant protein BCT. CCK8 used to analyzed the activity of EC after treated by different concentration of BCT. UPLC-MS/MS and ELISA used to detect themetabonomics and metabolites. The ability of migration and invasion was completed by transwell assay. RT-QPCR, WB used to analyze the expression of relevant genes. Results Our data showed that BCT was higher expression in EC tumor tissues (p < 0. 05) and BCT in 20 µg/mL promoted the survival, invasion and migration of EC cells (EC109) (p < 0. 05) . Meanwhile, UPLC-MS/MS results suggested that BCT resulted in an augmentation of hypotaurine metabolism, arachidonic acid metabolism, glycolysis/gluconeogenesis, tryptophan metabolism, citrate cycle activity in EC109 . The metabolic changes resulted in decreasing in glucose and pyruvate levels but increase in lactate dehydrogenase (LDH) activity and lactic acid (LA) as well as the expression of glucose transporter 1, Hexokinase 2, LDH which regulated the glycolysis were all changed (p < 0. 05) . The BCT treatment upregulated the expression ofTLR4, Akt, HIF-1α (p < 0. 05) which regulated the production of LA. Furthermore, LA stimulation promoted the expression of GPR81, Wnt, and β-catenin (p < 0. 05), thereby inducing EMT and metastasis in EC109 cells. Conclusion Altogether, these findings identified that impact of BCT in regulation of glycolysis in EC109 and its involves the TLR4/Akt/HIF-1α pathway. Meanwhile, glycolysis increasing the release of LA and promote the EMT of EC109 by GPR81/Wnt/β-catenin signaling pathway. In summary, our findings underscore the potential of targeting BCT as an innovative strategy to mitigate the development of EC. Keywords Fusobacterium periodonticum, Esophageal cancer, Glycolysi, TLR4/Akt/HIF-1α, EMT *Correspondence: Ran Liu [ranliu@seu.edu.cn](ranliu@seu.edu.cn) 1Key Laboratory of Environmental Medicine Engineering, School of Public Health, Ministry of Education, Southeast University, 87 Dingjiaqiao Street, Nanjing 210009, China © The Author(s) 2024. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit [http://creativecommons.org/l](http://creativecommons.org/l)icenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ([http:/

FAQs

What role does BCT from Fusobacterium periodonticum play in esophageal cancer cells?

BCT shows higher expression in esophageal cancer tumor tissues and enhances survival, invasion, and migration of esophageal cancer cells.

How does BCT alter glucose metabolism and lactate production?

BCT augments hypotaurine metabolism and glycolysis/gluconeogenesis, leading to decreased glucose and pyruvate while increasing LDH activity and lactic acid.

Which signaling pathways link BCT and lactic acid to EMT and metastasis?

BCT upregulates TLR4, Akt, and HIF-1α, which regulate lactic acid production; lactic acid then increases GPR81, Wnt, and β-catenin to induce EMT and metastasis.

Sep 22, 2026

Upload by Aurora