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Cancer-related gene expression analysis after treatment of prostate cancer cells with exercise-conditioned serum from advanced-stage prostate cancer patients after a 12-week WB-EMS training

ABSTRACT: We treated the prostate tumor cell line LNCaP with serum from prostate cancer patients that participated in a 12-week physical exercise and nutrional study. Exercise was conducted in form of whole-body electromyostimulation (WB-EMS). All patients from the control and the intervention group received nutritional counseling to achieve high-protein dietary intake (please refer to Schink, Herrmann et al, 2018; PMID: 30208857). Serum from all patients was taken at study entry and at the end of the intervention in week 12. Additionally, human primary skeletal muscle cells were treated with electric pulse stimulation to simulate in vitro exercise. EPS-conditioned medium was then also used to incubate prostate tumor cells. Treatment with either study patient serum or conditioned myotube medium was done for 24 h and for 72 h. Total RNA was isolated and cancer-related gene expression was analyzed using Nanostring technology.

ORGANISM(S): Homo sapiens

PROVIDER: GSE135541 | GEO | 2019/08/08

REPOSITORIES: GEO

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Project description:Cancer cells exhibit metabolic plasticity to meet oncogene-driven dependencies while coping with nutrient availability. A better understanding of how systemic metabolism impacts the accumulation of metabolites that reprogram the tumor microenvironment and drive cancer could facilitate development of precision nutrition approaches. Using the Hi-MYC prostate cancer mouse model, we demonstrated that an obesogenic high-fat diet rich in saturated fats accelerates the development of c-MYC-driven invasive prostate cancer through metabolic rewiring. Although c-MYC modulated key metabolic pathways, interaction with an obesogenic high-fat diet was necessary to induce glycolysis and lactate accumulation in tumors. These metabolic changes were associated with augmented infiltration of CD206+ and PD-L1+ tumor-associated macrophages and FOXP3+ regulatory T cells, as well as with the activation of transcriptional programs linked to disease progression and therapy resistance. Lactate itself also stimulated neoangiogenesis and prostate cancer cell migration, which were significantly reduced following treatment with the lactate dehydrogenase inhibitor FX11. In prostate cancer patients, high saturated fat intake and increased body mass index were associated with tumor glycolytic features that promote the infiltration of M2-like tumor-associated macrophages. Finally, upregulation of lactate dehydrogenase, indicative of a lactagenic phenotype, was associated with a shorter time to biochemical recurrence in independent clinical cohorts. This work identifies cooperation between genetic drivers and systemic metabolism to hijack the tumor microenvironment and promote prostate cancer progression through oncometabolite accumulation. This sets the stage for the assessment of lactate as a prognostic biomarker and supports strategies of dietary intervention and direct lactagenesis blockade in treating advanced prostate cancer. Murine prostate assays are reported in the current study MTBLS3317.Murine serum assays are reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS3316' rel='noopener noreferrer' target='_blank'>MTBLS3316</a>.

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Cancer-related gene expression analysis after treatment of prostate cancer cells with exercise-conditioned serum from advanced-stage prostate cancer patients after a 12-week WB-EMS training

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