Search bioRxiv⌕ Search

bioRxiv · 10.1101/2020.09.22.308056

Microbial metabolites of flavanols in urine are associated with enhanced anti-proliferative activity in bladder cancer cells in vitro

Abstract

Dietary flavanols and their metabolites are excreted primarily via the urine, suggesting uroepithelial cells as a site of activity due to lengthy exposure to high concentrations of these compounds. Flavanols are metabolized by the gut microbiota to numerous bioavailable metabolites. The observed effects of flavanols, including cancer chemoprevention, may be due in part to the activities of microbial metabolites. Most in vitro mechanistic work in this area relies on a limited pool of commercially available or synthesized flavanol microbial metabolites, and little work has been done in the area of bladder cancer. The impact of physiologically relevant mixtures of native flavanols and their metabolites generated in vivo remains unknown. Rats were fed various flavanols after which 48 h urine samples, approximating the total bioavailable metabolome, were collected. Urine samples were profiled by UPLC-MS/MS, and their anti-proliferative activities were assayed in vitro in four bladder cancer cell models. Significant interindividual variability was observed for chemical profiles and anti-proliferative activities. Concentrations of microbial metabolites (valerolactones, phenylalkyl acids and hippuric acids) were positively associated with reduced bladder cancer cell proliferation in vitro, while native flavanols were poorly correlated with activity. These results suggest that microbial metabolites may be the primary compounds responsible for chemoprevention in uroepithelial cell following flavanol consumption. Furthermore, this highlights the potential for exploiting knowledge about individual genetics, microbiome profiles, flavonoid metabolism profiles, tumor characteristics, etc. to design personalized dietary interventions for cancer prevention and/or adjuvant therapy to reduce bladder cancer incidence and improve outcomes.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Griffin, L. E., Kohrt, S. E., Rathore, A., Kay, C. D., Grabowska, M. M., Neilson, A. P.. 2020-09-23. Microbial metabolites of flavanols in urine are associated with enhanced anti-proliferative activity in bladder cancer cells in vitro. https://doi.org/10.1101/2020.09.22.308056

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Glycolysis and interferon transcription in melanoma immunotherapy

Glycolysis and interferon signalling have both been associated with responses to PD-1 blockade, but their joint transcriptional relationship with treatment outcome remains uncertain. We examined whether a state with high glycolysis and low interferon- response was associated with reduced disease control in melanoma. Fixed Hallmark gene sets were scored by single-sample gene set enrichment analysis in GSE91061, GSE78220 and an additional Liu cohort. Disease control analyses included 47, 26 and 100 patients. Conditional odds ratios for the joint state were 6.06 (exact 95% confidence interval, 1.04 to 65.61), 0.35 (0.026 to 3.11) and 1.03 (0.39 to 2.73), respectively. Holm-adjusted P values for the two initial comparisons were 0.073 and 0.365. The additional exploratory P value was 1.000. Continuous models and analyses that omitted each patient in turn did not provide consistent evidence of an adverse association. IFN scores were negatively correlated with DNA-derived tumour purity in 102 patients (Spearman {rho} = -0.671). Among 40 patients with paired biopsies, disease control was associated with higher on-treatment IFN scores after baseline adjustment, although the paired subset had lower baseline glycolysis than patients without paired profiles. In patient-level single-cell analyses, the baseline CD8 T cell correlation weakened when an alternative rank score used a common gene background. The defined joint state was not consistently associated with poorer disease control across cohorts. Bulk IFN scores were related to tumour purity, and cellular correlations were sensitive to scoring choices. These transcriptomic results do not measure pyruvate concentration, glycolytic flux or STAT1 pyruvylation.

cancer biology↗

Psychoneuroimmunology of Viral Hepatitis and Hepatocellular Carcinoma: A Systematic Review and Meta-Analysis

Hepatocellular carcinoma (HCC) and viral hepatitis (VH) are recognized primarily as hepatic diseases, yet they impose a substantial neuropsychiatric disorders (NPDs) encompassing depression, anxiety, cognitive impairment, and fatigue. Whether these manifestations reflect psychological reactions or biologically grounded psychoneuroimmune dysfunction remains poorly understood. Here, we present a pre-registered systematic review and meta-analysis (PROSPERO 2026 CRD420251081757) synthesizing evidence from 24 studies combining psychosocial outcomes with immune dysregulation markers across HCC and VH populations. Bibliometric and network analyses identified a growing psychoneuroimmunology research hub linking cytokine signaling, microglial activation, blood-brain barrier (BBB) disruption, and gut-liver-brain axis dysregulation to the neuropsychiatric phenotype of these diseases. Meta-analysis revealed a pooled hazard ratio (HR) of 1.92 (95% CI: 1.09-3.39) for adverse outcomes in HCC and a pooled HR of 2.28 (95% CI: 1.48-3.52) for depression associated to genetic variants in VH. TNF-a, but not IL-6, showed a tendency toward lower levels in VH patients with versus without NPDs, suggesting differential inflammatory roles. The literature, however, remains fragmented by heterogeneous designs and a paucity of longitudinal data. A psychoneuroimmunological approach, integrating immune, endocrine, neural, and psychosocial dimensions, is essential for capturing the full systemic impact of HCC and VH and should inform future mechanistic research and multidisciplinary clinical strategies.

cancer biology↗

Nutrient Availability as a Driver of Transcriptome Reprogramming in Osteosarcoma

Background: Gene expression in mammalian cells is intricately regulated by environmental and metabolic cues. Among these, nutrient availability represents a key feature of the tumor microenvironment and has recently emerged as a potent modulator of oncogenic signaling networks. In this study, we employed a cell-line model of osteosarcoma, a rare but highly aggressive bone malignancy affecting both humans and dogs. We demonstrate that altering the concentration of a single nutrient can profoundly reprogram gene expression in osteosarcoma cells, revealing a previously underexplored phenomenon: nutrient-dependent gene regulation. This finding highlights potential opportunities for therapeutic intervention and underscores the broader implications of metabolic regulation for personalized medicine and nutrition. Methods/Results: We performed bulk RNA sequencing of an established osteosarcoma cell line cultured under varying concentrations of two key nutrients, glucose and glutamine. Differential gene expression analysis revealed a pronounced nutrient-dependent transcriptional response. The identified genes were functionally associated with pathways involved in cancer, development, nervous system regulation, metabolism, cellular signaling, and immune responses. We identified seven distinct expression patterns, one of which exhibited a striking correlation with cell growth rate and resembled a FOS-like transcriptional signature. Notably, the proto-oncogene FOS was among the identified genes and displayed a strong growth-rate-dependent expression pattern. Conclusion/Impact: Our findings demonstrate that modulation of nutrient availability profoundly reshapes the gene expression landscape of osteosarcoma cells, revealing nutrient-responsive targets with potential therapeutic relevance. This work expands our understanding of metabolic regulation in cancer and suggests that nutrient-based interventions may provide a controllable means of influencing tumor progression. Beyond oncology, such approaches may also have broader implications for developmental biology, autoimmune disorders, and nervous system function. More broadly, this study highlights the potential of metabolic interventions as a strategy for targeted modulation of gene expression programs.

cancer biology↗