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Published on: May 11, 2016
Propionibacterium acnes inhibits FOXM1 and induces cell cycle alterations in human primary prostate cells
Behnam Sayanjali1, Gitte J M Christensen2, Munir A Al-Zeer1
1Department of Molecular Biology, Max Planck Institute of Infection Biology, Berlin, Germany.
Abstract:
Propionibacterium acnes has been detected in diseased human prostate tissue, and cell culture experiments suggest that the bacterium can establish a low-grade inflammation. Here, we investigated its impact on human primary prostate epithelial cells. Microarray analysis confirmed the inflammation-inducing capability of P. acnes but also showed deregulation of genes involved in the cell cycle. qPCR experiments showed that viable P. acnes downregulates a master regulator of cell cycle progression, FOXM1. Flow cytometry experiments revealed that P. acnes increases the number of cells in S-phase. We tested the hypothesis that a P. acnes-produced berninamycin-like thiopeptide is responsible for this effect, since it is related to the FOXM1 inhibitor siomycin. The thiopeptide biosynthesis gene cluster was strongly expressed; it is present in subtype IB of P. acnes, but absent from type IA, which is most abundant on human skin. A knock-out mutant lacking the gene encoding the berninamycin-like peptide precursor was unable to downregulate FOXM1 and to halt the cell cycle. Our study reveals a novel host cell-interacting activity of P. acnes.
Insights
Propionibacterium acnes, a bacterium found in prostate tissue, disrupts the cell cycle by downregulating FOXM1. A specific peptide produced by P. acnes is responsible for this effect, impacting cell cycle progression.
Area of Science:
- Microbiology
- Cell Biology
- Prostate Cancer Research
Background:
- Propionibacterium acnes (P. acnes) is linked to diseased human prostate tissue and can cause inflammation.
- Previous studies suggest P. acnes may influence cellular processes beyond inflammation.
Purpose of the Study:
- To investigate the impact of P. acnes on human primary prostate epithelial cells.
- To identify the specific mechanisms by which P. acnes affects the cell cycle.
Main Methods:
- Microarray analysis to assess gene expression changes.
- Quantitative PCR (qPCR) to measure FOXM1 gene expression.
- Flow cytometry to analyze cell cycle phases.
- Genetic manipulation of P. acnes to create a knock-out mutant.
Main Results:
- P. acnes confirmed to induce inflammation and deregulate cell cycle genes.
- Viable P. acnes downregulates FOXM1, a key cell cycle regulator.
- P. acnes increases the proportion of cells in S-phase.
- A berninamycin-like thiopeptide produced by P. acnes subtype IB is responsible for FOXM1 downregulation and cell cycle arrest.
- A knock-out mutant lacking this peptide could not downregulate FOXM1 or halt the cell cycle.
Conclusions:
- P. acnes possesses a novel mechanism to interact with host cells by modulating the cell cycle.
- A specific thiopeptide produced by P. acnes subtype IB plays a critical role in this interaction.
- This finding offers new insights into the role of P. acnes in prostate health and disease.
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