Journal Article

DKFZ-2026-02545

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Gemella morbillorum promotes colorectal tumorigenesis through barrier disruption and invasion-dependent DNA damage.

Meyers, M. ; Medina Evora, G. ; Molina Tijeras, J. A. ; Brauer, M. ; Benzarti, M. ; Jans, M. ; Delgado, L. F. ; Schorr, L.DKFZ* ; Rodriguez, F. ; Ternes, D. ; Ouyang, K. S.DKFZ* ; Moskal, K.DKFZ* ; Schlicker, L. ; Tsenkova, M. ; Lucchetti, M. ; Gilson, C. ; Gabola, M. ; Carpentier, A. ; Nuciforo, P. G. ; Koncina, E. ; Pozdeev, V. I. ; Vereecke, L. ; Wilmes, P. ; Puschhof, J.DKFZ* ; Letellier, E.

2026
Elsevier Amsterdam [u.a.]

Abstract: Bacteria are increasingly recognized as contributors to cancer, yet the underlying mechanisms remain unclear for most species. Here, we find that Gemella morbillorum (Gm) is enriched in feces and tumor tissues from patients with colorectal cancer (CRC) and reveal a multi-step host-pathogen mechanism that promotes colorectal tumorigenesis. In mouse models of CRC, Gm suppresses IL-22 production by type 3 innate lymphoid cells (ILC3s), impairing intestinal barrier function and facilitating bacterial translocation to early neoplastic lesions. At the tumor site, Gm utilizes an ANXA2-dependent, clathrin-mediated pathway to invade CRC cells. Gm induces profound lipid remodeling, characterized by the accumulation of oxidation-prone fatty acids and enhanced lipid peroxidation, which contributes to invasion-dependent DNA damage. Inhibition of lipid peroxidation attenuates Gm-induced DNA damage, functionally linking lipid oxidative stress to genotoxicity. Together, these findings identify Gm as a candidate onco-pathogen in CRC that uses multiple mechanisms to disarm the intestinal barrier and trigger genotoxicity.

Keyword(s): DNA damage ; Gemella morbillorum ; IL-22 ; colorectal cancer ; gut barrier integrity ; invasive bacterium ; lipid peroxidation ; lipid remodeling ; tumor microbiome ; type 3 innate lymphoid cells

Note: epub

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Contributing Institute(s):

1. NWG Epithel-Mikrobiom-Interaktionen (D300)
2. DKTK HD zentral (HD01)

Research Program(s):

1. 314 - Immunologie und Krebs (POF4-314) (POF4-314)

Appears in the scientific report 2026

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Database coverage:
; BIOSIS Previews ; Biological Abstracts ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; Essential Science Indicators ; IF >= 30 ; JCR ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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