The effects of biofilms on tumor progression in a 3D cancer-biofilm microfluidic model

Deng, Yanlin; Liu, Sylvia Yang; Chua, Song Lin; Khoo, Bee Luan

doi:10.1016/j.bios.2021.113113

Cited by 27 publications

(13 citation statements)

References 72 publications

(80 reference statements)

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“…Chronic inflammation has been linked to many carcinogenesis stages, 25,26 and biofilm formation has been attributed to a potential etiological role in the development of some cancers. [27][28][29] Recent clinical studies have linked fungi (e.g., C. albicans) and cancer, claiming the need for more in vitro and in vivo studies in this area. 30,31 In a tumor microenvironment, the resident microbiota and its metabolites trigger metabolic signaling pathways, which further promote or suppress the malignant behavior of host cells.…”

Section: Discussionmentioning

confidence: 99%

Extracellular lipids of Candida albicans biofilm induce lipid droplet formation and decreased response to a topoisomerase I inhibitor in dysplastic and neoplastic oral cells

et al. 2022

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Extracellular lipids of Candida albicans biofilm induce lipid droplet formation and decreased response to a topoisomerase I inhibitor in dysplastic and neoplastic oral cells* Objective: Some microorganisms, i.e., Candida albicans, have been associated with cancer onset and development, although whether the fungus promotes cancer or whether cancer facilitates the growth of C. albicans is unclear. In this context, microbial-derived molecules can modulate the growth and resistance of cancer cells. This study isolated extracellular lipids (ECL) from a 36-h Candida albicans biofilm incubated with oral dysplastic (DOK) and neoplastic (SCC 25) cells, which were further challenged with the topoisomerase I inhibitor camptothecin (CPT), a lipophilic anti-tumoral molecule. Methodology: ECL were extracted from a 36-h Candida albicans biofilm with the methanol/chloroform precipitation method and identified with Nuclear Magnetic Resonance (1H-NMR). The MTT tetrazolium assay measured ECL cytotoxicity in DOK and SCC 25 cells, alamarBlue™ assessed cell metabolism, flow cytometry measured cell cycle, and confocal microscopy determined intracellular features. Results: Three major classes of ECL of C. albicans biofilm were found: phosphatidylinositol (PI), phosphatidylcholine (PC), and phosphatidylglycerol (PG). The ECL of C. albicans biofilm had no cytotoxic effect on neither cell after 24 hours, with a tendency to disturb the SCC 25 cell cycle profile (without statistical significance). The ECL-induced intracellular lipid droplet (LD) formation on both cell lines after 72 hours. In this context, ECL enhanced cell metabolism, decreased the response to CPT, and modified intracellular drug distribution. Conclusion: The ECL (PI, PC, and PG) of 36-h Candida albicans biofilm directly interacts with dysplastic and neoplastic oral cells, highlighting the relevance of better understanding C. albicans biofilm signaling in the microenvironment of tumor cells.

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Section: Discussionmentioning

confidence: 99%

Extracellular lipids of Candida albicans biofilm induce lipid droplet formation and decreased response to a topoisomerase I inhibitor in dysplastic and neoplastic oral cells

et al. 2022

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“…Cells can form compact clusters in our tapered microwell assay (Supplementary Figure 3). Besides, the inside walls of our microwell could provide sufficient depth to avoid turbulence incurred from media change while concentrating the cells for cluster formation [16] , [18] , [19] , [20] , [66] .…”

Section: Methodsmentioning

confidence: 99%

Oxidative stress induced by Etoposide anti-cancer chemotherapy drives the emergence of tumor-associated bacteria resistance to fluoroquinolones

Wang

Chan

Deng³

et al. 2024

Journal of Advanced Research

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“…As optimized in our previous study, the resulting cluster size range would be clinically comparable to large cancer microclusters in vivo (≈50 cells). [30,31] To mimic the different co-localization of infectious bacteria within the TME, we first established a coating (CT) model with extratumoral bacterial aggregates using human-derived uropathogenic Escherichia coli (UPEC) strain UTI89 and colonizing (CL) model with infiltrating bacteria, respectively. UTI89 infection in the form of EBs or intratumoral bacteria (IB) strains was performed at a multiplicity of infection (MOI) rate (human cells: bacteria) of 1:1 for clinical relevance.…”

Section: Development Of the Tam Pieb Microfluidic Tumor Bacterial Mod...mentioning

confidence: 99%

“…We previously reported that biofilms promote cancer progression through cancer stem cells (CSCs) and induce higher chemoresistance in bladder cancer. [30] Here, we developed a novel cancer inflammation model (TAM PIEB ) that revealed the unique interactions of TAMs with bladder cancer cells in the presence of human-derived uropathogenic Escherichia coli (UPEC) strain UTI89. The integrated microfluidic-based tumor inflammatory model enabled in situ analysis and drug screening of TAM-tumor-bacteria 3D models.…”

Section: Introductionmentioning

confidence: 99%

Biofilm Potentiates Cancer‐Promoting Effects of Tumor‐Associated Macrophages in a 3D Multi‐Faceted Tumor Model

Deng

Chua

et al. 2023

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Components of the tumor microenvironment (TME), such as tumor‐associated macrophages (TAMs), influence tumor progression. The specific polarization and phenotypic transition of TAMs in the tumor microenvironment lead to two‐pronged impacts that can promote or hinder cancer development and treatment. Here, a novel microfluidic multi‐faceted bladder tumor model (TAMPIEB) is developed incorporating TAMs and cancer cells to evaluate the impact of bacterial distribution on immunomodulation within the tumor microenvironment in vivo. It is demonstrated for the first time that biofilm‐induced inflammatory conditions within tumors promote the transition of macrophages from a pro‐inflammatory M1‐like to an anti‐inflammatory/pro‐tumor M2‐like state. Consequently, multiple roles and mechanisms by which biofilms promote cancer by inducing pro‐tumor phenotypic switch of TAMs are identified, including cancer hallmarks such as reducing susceptibility to apoptosis, enhancing cell viability, and promoting epithelial‐mesenchymal transition and metastasis. Furthermore, biofilms formed by extratumoral bacteria can shield tumors from immune attack by TAMs, which can be visualized through various imaging assays in situ. The study sheds light on the underlying mechanism of biofilm‐mediated inflammation on tumor progression and provides new insights into combined anti‐biofilm therapy and immunotherapy strategies in clinical trials.

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The effects of biofilms on tumor progression in a 3D cancer-biofilm microfluidic model

Cited by 27 publications

References 72 publications

Extracellular lipids of Candida albicans biofilm induce lipid droplet formation and decreased response to a topoisomerase I inhibitor in dysplastic and neoplastic oral cells

Extracellular lipids of Candida albicans biofilm induce lipid droplet formation and decreased response to a topoisomerase I inhibitor in dysplastic and neoplastic oral cells

Oxidative stress induced by Etoposide anti-cancer chemotherapy drives the emergence of tumor-associated bacteria resistance to fluoroquinolones

Biofilm Potentiates Cancer‐Promoting Effects of Tumor‐Associated Macrophages in a 3D Multi‐Faceted Tumor Model

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