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Published on: July 28, 2010
Periodontitis-Associated Circulating EVs Promote Colorectal Cancer Progression via Carnosine-Mediated Acidosis
Ruoyi Wu1, Zihan Cai1, Hualing Sun1
1State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Cell Proliferation
|July 1, 2026
Summary
Periodontitis (PD) accelerates colorectal cancer (CRC) by releasing extracellular vesicles (EVs) that deliver carnosine. These periodontitis-associated EVs (PDEVs) promote tumor growth and adaptation to acidic environments, offering potential therapeutic targets.
Area of Science:
- Oncology
- Microbiology
- Biochemistry
Background:
- Colorectal cancer (CRC) is a leading global malignancy.
- Epidemiological studies suggest a link between periodontitis (PD) and increased CRC risk.
- The underlying mechanisms connecting PD and CRC remain largely unknown.
Purpose of the Study:
- To investigate the role of extracellular vesicles (EVs) in mediating the relationship between PD and CRC.
- To elucidate the functional contribution and cargo of periodontitis-associated EVs (PDEVs) in CRC progression.
Main Methods:
- Established a PD model in Apc+/- mice with spontaneous intestinal tumorigenesis.
- Isolated and characterized circulating EVs from PD mice.
- Utilized pharmacological inhibition of EV release and MC38 syngeneic tumor models.
- Performed metabolomic profiling, RNA sequencing, and in vitro assays.
Main Results:
- PD significantly accelerated CRC onset and increased tumor burden in mice.
- Inhibition of EV release attenuated PD-driven tumor progression, highlighting the role of PDEVs.
- PDEVs promoted tumor growth, induced an immunosuppressive tumor microenvironment, and were enriched in carnosine.
- EV-delivered carnosine aided tumor cell adaptation to acidic conditions, promoting proliferation and migration.
Conclusions:
- Circulating EVs mediate a metabolic communication pathway linking PD to CRC progression.
- PDEVs deliver carnosine, supporting malignant phenotypes and tumor adaptation to acidic stress.
- EV-associated carnosine presents a potential biomarker and therapeutic target for CRC modulation.
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