Cutibacterium acnes invades prostate epithelial cells to induce BRCAness as a possible pathogen of prostate cancer

Author:

Ashida Shingo1ORCID,Kawada Chiaki1,Tanaka Hiroko2,Kurabayashi Atsushi3,Yagyu Ken‐ichi4,Sakamoto Shuji5,Maejima Kazuhiro6,Miyano Satoru2ORCID,Daibata Masanori7,Nakagawa Hidewaki6,Inoue Keiji1

Affiliation:

1. Department of Urology Kochi Medical School Nankoku Japan

2. M&D Data Science Center Tokyo Medical and Dental University Tokyo Japan

3. Department of Pathology Kochi Medical School Nankoku Japan

4. Division of Biological Research, Science Research Center Kochi Medical School Nankoku Japan

5. Laboratory of Molecular Biology, Science Research Center Kochi Medical School Nankoku Japan

6. Laboratory for Cancer Genomics RIKEN Center for Integrative Medical Sciences Yokohama Japan

7. Department of Microbiology and Infection Kochi Medical School Nankoku Japan

Abstract

AbstractBackgroundAbundant evidence suggests that chronic inflammation is linked to prostate cancer and that infection is a possible cause of prostate cancer.MethodsTo identify microbiota or pathogens associated with prostate cancer, we investigated the transcriptomes of 20 human prostate cancer tissues. We performed de novo assembly of nonhuman sequences from RNA‐seq data.ResultsWe identified four bacteria as candidate microbiota in the prostate, including Moraxella osloensis, Uncultured chroococcidiopsis, Cutibacterium acnes, and Micrococcus luteus. Among these, C. acnes was detected in 19 of 20 prostate cancer tissue samples by immunohistochemistry. We then analyzed the gene expression profiles of prostate epithelial cells infected in vitro with C. acnes and found significant changes in homologous recombination (HR) and the Fanconi anemia pathway. Notably, electron microscopy demonstrated that C. acnes invaded prostate epithelial cells and localized in perinuclear vesicles, whereas analysis of γH2AX foci and HR assays demonstrated impaired HR repair. In particular, BRCA2 was significantly downregulated in C. acnes–infected cells.ConclusionsThese findings suggest that C. acnes infection in the prostate could lead to HR deficiency (BRCAness) which promotes DNA double‐strand breaks, thereby increasing the risk of cancer development.

Publisher

Wiley

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