Recent advances in metabolomics of triple negative breast cancer

Kumari, Seema; Malla, Rama Rao

doi:10.1111/tbj.13524

Cited by 6 publications

(3 citation statements)

References 32 publications

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“…These metabolites exert antineoplastic effects, including modulation of cell proliferation and epithelial-mesenchymal transition (EMT) [44]. As stated earlier, the metabolic capacity of the microbiome is suppressed in breast cancer, and the capacity to produce known antineoplastic metabolites decreases in breast cancer [29][30][31][45][46][47].…”

Section: Introductionmentioning

confidence: 93%

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Identification of Bacterial Metabolites Modulating Breast Cancer Cell Proliferation and Epithelial-Mesenchymal Transition

Ujlaki,

Kovács,

Vida

et al. 2023

Molecules

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Breast cancer patients are characterized by the oncobiotic transformation of multiple microbiome communities, including the gut microbiome. Oncobiotic transformation of the gut microbiome impairs the production of antineoplastic bacterial metabolites. The goal of this study was to identify bacterial metabolites with antineoplastic properties. We constructed a 30-member bacterial metabolite library and screened the library compounds for effects on cell proliferation and epithelial-mesenchymal transition. The metabolites were applied to 4T1 murine breast cancer cells in concentrations corresponding to the reference serum concentrations. However, yric acid, glycolic acid, d-mannitol, 2,3-butanediol, and trans-ferulic acid exerted cytostatic effects, and 3-hydroxyphenylacetic acid, 4-hydroxybenzoic acid, and vanillic acid exerted hyperproliferative effects. Furthermore, 3-hydroxyphenylacetic acid, 4-hydroxybenzoic acid, 2,3-butanediol, and hydrocinnamic acid inhibited epithelial-to-mesenchymal (EMT) transition. We identified redox sets among the metabolites (d-mannitol—d-mannose, 1-butanol—butyric acid, ethylene glycol—glycolic acid—oxalic acid), wherein only one partner within the set (d-mannitol, butyric acid, glycolic acid) possessed bioactivity in our system, suggesting that changes to the local redox potential may affect the bacterial secretome. Of the nine bioactive metabolites, 2,3-butanediol was the only compound with both cytostatic and anti-EMT properties.

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Section: Introductionmentioning

confidence: 93%

“…Oncobiosis support of breast tumors is multifaceted. (1) Bacteria colonize the tumor tissue; (2) the immune system favors the tolerogenic state [44]; and (3) the gut microbiome's capacity to produce antitumor metabolites is suppressed [29][30][31][45][46][47].…”

Section: Introductionmentioning

confidence: 99%

Identification of Bacterial Metabolites Modulating Breast Cancer Cell Proliferation and Epithelial-Mesenchymal Transition

Ujlaki,

Kovács,

Vida

et al. 2023

Molecules

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“…As the gut microbiome is the biggest in the body in terms of the number of bacteria, its metabolic capacity is considerable. The biosynthetic capacity of the oncobiome is suppressed compared to the eubiome [ 126 , 127 ]. Multiple bioactive bacterial metabolites were identified that can modulate the behavior of breast cancer cells (Table 3 ).…”

Section: Interactions Between the Oncobiome Tumors And Tumor Cellsmentioning

confidence: 99%

The involvement of oncobiosis and bacterial metabolite signaling in metastasis formation in breast cancer

Kovàcs

Mikó

Ujlaki

et al. 2021

Cancer Metastasis Rev

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Breast cancer, the most frequent cancer in women, is characterized by pathological changes to the microbiome of breast tissue, the tumor, the gut, and the urinary tract. Changes to the microbiome are determined by the stage, grade, origin (NST/lobular), and receptor status of the tumor. This year is the 50th anniversary of when Hill and colleagues first showed that changes to the gut microbiome can support breast cancer growth, namely that the oncobiome can reactivate excreted estrogens. The currently available human and murine data suggest that oncobiosis is not a cause of breast cancer, but can support its growth. Furthermore, preexisting dysbiosis and the predisposition to cancer are transplantable. The breast’s and breast cancer’s inherent microbiome and the gut microbiome promote breast cancer growth by reactivating estrogens, rearranging cancer cell metabolism, bringing about a more inflammatory microenvironment, and reducing the number of tumor-infiltrating lymphocytes. Furthermore, the gut microbiome can produce cytostatic metabolites, the production of which decreases or blunts breast cancer. The role of oncobiosis in the urinary tract is largely uncharted. Oncobiosis in breast cancer supports invasion, metastasis, and recurrence by supporting cellular movement, epithelial-to-mesenchymal transition, cancer stem cell function, and diapedesis. Finally, the oncobiome can modify the pharmacokinetics of chemotherapeutic drugs. The microbiome provides novel leverage on breast cancer that should be exploited for better management of the disease.

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