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Ignatova, Nadezhda, Pryazhnikova, Maria, Seliverstov, Andrey, Abidullina, Alina, Gamayunov, Sergey, Shirmanova, Marina, Druzhkova, Irina. (1404). Effects of Tumor-associated E. coli Metabolites on Migration of Colorectal Cancer Cells. سامانه مدیریت نشریات علمی, 80(6), 1621-1632. doi: 10.66224/ARI.80.6.3499
Nadezhda Ignatova; Maria Pryazhnikova; Andrey Seliverstov; Alina Abidullina; Sergey Gamayunov; Marina Shirmanova; Irina Druzhkova. "Effects of Tumor-associated E. coli Metabolites on Migration of Colorectal Cancer Cells". سامانه مدیریت نشریات علمی, 80, 6, 1404, 1621-1632. doi: 10.66224/ARI.80.6.3499
Ignatova, Nadezhda, Pryazhnikova, Maria, Seliverstov, Andrey, Abidullina, Alina, Gamayunov, Sergey, Shirmanova, Marina, Druzhkova, Irina. (1404). 'Effects of Tumor-associated E. coli Metabolites on Migration of Colorectal Cancer Cells', سامانه مدیریت نشریات علمی, 80(6), pp. 1621-1632. doi: 10.66224/ARI.80.6.3499
Ignatova, Nadezhda, Pryazhnikova, Maria, Seliverstov, Andrey, Abidullina, Alina, Gamayunov, Sergey, Shirmanova, Marina, Druzhkova, Irina. Effects of Tumor-associated E. coli Metabolites on Migration of Colorectal Cancer Cells. سامانه مدیریت نشریات علمی, 1404; 80(6): 1621-1632. doi: 10.66224/ARI.80.6.3499

Effects of Tumor-associated E. coli Metabolites on Migration of Colorectal Cancer Cells

Archives of Razi Institute
مقاله 28، دوره 80، شماره 6، بهمن و اسفند 2025، صفحه 1621-1632    اصل مقاله (2.78 M)
نوع مقاله: Original Articles
شناسه دیجیتال (DOI): 10.66224/ARI.80.6.3499
نویسندگان
Nadezhda Ignatova* 1؛ Maria Pryazhnikova2؛ Andrey Seliverstov3؛ Alina Abidullina2؛ Sergey Gamayunov4؛ Marina Shirmanova2؛ Irina Druzhkova2
1Department of Epidemiology, Microbiology and Evidence-Based Medicine, Privolzhsky Research Medical University, Nizhny Novgorod, Russia.
2Institute of Experimental Oncology and Biomedical Technologies, Privolzhsky Research Medical University, Nizhny Novgorod, Russia.
3Central Research Laboratory, Privolzhsky Research Medical University, Nizhny Novgorod, Russia.
4Nizhny Novgorod Regional Oncologic Hospital, Nizhny Novgorod, Russia.
چکیده
Introduction: Colorectal tumors have a close connection with the gut microbiome. A correlation between rearrangement in microbiome composition and disease progression has already been shown. However, the mechanisms underlying interactions between microorganisms and cancer cells, as well as the immediate effects of tumor-associated microbiomes on cancer cells, remain unclear.
Materials & Methods: In this work, we investigated the effects of metabolites produced by tumor-associated Escherichia coli strains on the migration of human colorectal cancer cell lines (HCT116, SW480 and HT29).
Results: We identified differences in some biochemical enzyme activity of E. coli strains and in the spectrum of synthesized organic acids between tumor-associated strains and the probiotic E. coli M-17 strains. Most strains associated with colorectal cancer were unable to utilize sucrose. Specifically, tumor-associated E. coli produced more fumaric, malic and maleic acids, whereas the E. coli M-17 produced more short-chain fatty acids such as propionic, 2-oxobutyric, and α-ketoglutaric acids (AKGs). Upon exposure to metabolites from tumor-associated E. coli strains, HCT116 and SW480 cells showed an increased migration activity, whereas HT29 cells showed decreased migration activity in both 2D and 3D culture models. Immunocytochemistry assay revealed a decrease in E-cadherin in HCT116 and SW480 cells and focal adhesion kinase (FAK)- in HT29, which explains the different effects of E. coli metabolites on migratory capacity of colorectal cancer cells. 
Conclusion: Therefore, these results suggest that the effect of tumor-associated E. coli strains on cancer cells migration depends on their innate type of migration and enhances FAK-dependent single-cell migration accompanied by the loss of E-cadherin in cancer cells with initially low FAK expression. In contrast, this effect was not observed in cancer cells exhibiting a collective migration phenotype.
کلیدواژه‌ها
Escherichia coli؛ Metabolites؛ Colon cancer؛ Migration
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References

  1. Falih Soliman N, Jasim Mohamad B. Clinical and histopathological characteristics of colorectal cancer in Iraq between 2015-2021. Arch Razi Inst. 2022; 77(6):2407-13. [DOI:10.22092/ARI.2022.358613.2263] [PMID]
  2. Kim J, Lee HK. Potential role of the gut microbiome in colorectal cancer progression. Front Immunol. 2022; 12:807648. [DOI:10.3389/fimmu.2021.807648] [PMID]
  3. Leylabadlo HE, Ghotaslou R, Feizabadi MM, Farajnia S, Moaddab SY, Ganbarov K, et al. The critical role of Faecalibacterium prausnitzii in human health: An overview. Microb Pathog. 2020; 149:104344. [DOI:10.1016/j.micpath.2020.104344] [PMID]
  4. Ahmad Kendong SM, Raja Ali RA, Nawawi KNM, Ahmad HF, Mokhtar NM. Gut dysbiosis and intestinal barrier dysfunction: Potential explanation for early-onset colorectal cancer. Front Cell Infect Microbiol. 2021; 11:744606. [DOI:10.3389/fcimb.2021.744606] [PMID]
  5. Chen K, McCulloch J, Das Neves R, Rodrigues G, Hsieh WT, Gong W, et al. The beneficial effects of commensal E. coli for colon epithelial cell recovery are related with Formyl peptide receptor 2 (Fpr2) in epithelial cells. Gut Pathog. 2023; 15(1):28.[DOI:10.1186/s13099-023-00557-w] [PMID]
  6. Lichtenstern CR, Lamichhane-Khadka R. A tale of two bacteria - Bacteroides fragilis, Escherichia coli, and colorectal cancer. Front Bacteriol. 2023; 2:1229077. [DOI:10.3389/fbrio.2023.1229077]
  7. Mohamed ET, Mundhada H, Landberg J, Cann I, Mackie RI, Nielsen AT, et al. Generation of an E. coli platform strain for improved sucrose utilization using adaptive laboratory evolution. Microb Cell Fact. 2019; 18(1):116. [DOI:10.1186/s12934-019-1165-2] [PMID]
  8. Goubet AG. Could the tumor-associated microbiota be the new multi-faceted player in the tumor microenvironment? Front Oncol. 2023; 13:1185163. [DOI:10.3389/fonc.2023.1185163] [PMID]
  9. Schorr L, Mathies M, Elinav E, Puschhof J. Intracellular bacteria in cancer-prospects and debates. NPJ Biofilms Microbiomes. 2023; 9(1):76. [DOI:10.1038/s41522-023-00446-9] [PMID]
  10. Kaźmierczak-Siedlecka K, Marano L, Merola E, Roviello F, Połom K. Sodium butyrate in both prevention and supportive treatment of colorectal cancer. Front Cell Infect Microbiol. 2022; 12:1023806. [DOI:10.3389/fcimb.2022.1023806] [PMID]
  11. Bordonaro M. Further analysis of p300 in mediating effects of Butyrate in Colorectal Cancer Cells. J Cancer. 2020; 11(20):5861-6. [DOI:10.7150/jca.47160] [PMID]
  12. Orlov YP, Butrov AV, Sviridov SV, Afanasyev VV, Kondratiev AN, Tsentsiper LM, et al. Succinate and succinate dehydrogenase as a “fulcrum” in the Krebs cycle in critical conditions. Antibiot Chemother. 2023; 68(1-2):57-68. [DOI:10.37489/0235-2990-2023-68-1-2-57-68]
  13. Sica V, Bravo-San Pedro JM, Izzo V, Pol J, Pierredon S, Enot D, et al. Lethal poisoning of cancer cells by respiratory chain inhibition plus dimethyl α-Ketoglutarate. Cell Rep. 2019; 27(3):820-34.e9. [DOI:10.1016/j.celrep.2019.03.058] [PMID]
  14. Xi Y, Jing Z, Wei W, Chun Z, Quan Q, Qing Z, et al. Inhibitory effect of sodium butyrate on colorectal cancer cells and construction of the related molecular network. BMC Cancer. 2021; 21(1):127. [DOI:10.1186/s12885-021-07845-1] [PMID]
  15. Zheng L, Zhu ZR, Sneh T, Zhang WT, Wang ZY, Wu GY, et al. Circulating succinate-modifying metabolites accurately classify and reflect the status of fumarate hydratase-deficient renal cell carcinoma. J Clin Invest. 2023; 133(11):e165028. [DOI:10.1172/JCI165028] [PMID]
  16. Roupar D, González A, Martins JT, Gonçalves DA, Teixeira JA, Botelho C, et al. Modulation of Designed Gut Bacterial Communities by Prebiotics and the Impact of Their Metabolites on Intestinal Cells. Foods. 2023; 12(23):4216.[DOI:10.3390/foods12234216] [PMID]
  17. Baryła M, Semeniuk-Wojtaś A, Róg L, Kraj L, Małyszko M, Stec R. Oncometabolites-A link between cancer cells and tumor microenvironment. biology (Basel). 2022; 11(2):270. [DOI:10.3390/biology11020270] [PMID]
  18. Ternes D, Tsenkova M, Pozdeev VI, Meyers M, Koncina E, Atatri S, et al. The gut microbial metabolite formate exacerbates colorectal cancer progression. Nat Metab. 2022; 4(4):458-75. [DOI:10.1038/s42255-022-00558-0] [PMID]
  19. Sciacovelli M, Gonçalves E, Johnson TI, Zecchini VR, da Costa AS, Gaude E, et al. Fumarate is an epigenetic modifier that elicits epithelial-to-mesenchymal transition. Nature. 2016; 537(7621):544-7. [DOI:10.1038/nature19353] [PMID]
  20. He J, Han Z, Luo W, Shen J, Xie F, Liao L, et al. Serum organic acid metabolites can be used as potential biomarkers to identify prostatitis, benign prostatic hyperplasia, and prostate cancer. Front Immunol. 2023; 13:998447. [DOI:10.3389/fimmu.2022.998447] [PMID]
  21. Lu YW, Hou XL, Koo HM, Chao WT. Dasatinib suppresses collective cell migration through the coordination of focal adhesion and E-cadherin in colon cancer cells. Heliyon. 2023; 10(1):e23501 [DOI:10.1016/j.heliyon.2023.e23501] [PMID]
  22. Tarashi S, Siadat SD, Ahmadi Badi S, Zali M, Biassoni R, Ponzoni M, et al. Gut bacteria and their metabolites: Which one is the defendant for colorectal cancer? Microorganisms. 2019; 7(11):561 [DOI:10.3390/microorganisms7110561] [PMID]
  23. Thirunavukkarasan M, Wang C, Rao A, Hind T, Teo YR, Siddiquee AA, et al. Short-chain fatty acid receptors inhibit invasive phenotypes in breast cancer cells. Plos One. 2017; 12(10):e0186334. [DOI:10.1371/journal.pone.0186334] [PMID]
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