Intratumoral Parvimonas micra promotes esophageal squamous cell carcinoma via p-cresol–induced Treg differentiation
Menée à l'aide de 119 échantillons tumoraux et 119 échantillons tissulaires normaux provenant de patients atteints d'un carcinome épidermoïde de l'oesophage, cette étude met en évidence un mécanisme par lequel la bactérie Parvimonas micra favorise la croissance tumorale via la sécrétion du p-crésol, un métabolite issu de la fermentation des acides aminés, l'accroissement du niveau des espèces réactives de l'oxygène et la différenciation des lymphocytes T régulateurs FOXP3+
Intratumoral microbiota has emerged as a notable factor influencing cancer initiation and progression. However, its composition and functional impact in esophageal squamous cell carcinoma (ESCC) remain largely unexplored. Here, we performed metagenomic sequencing on 119 paired tumor-normal tissues from patients with ESCC and single-cell RNA sequencing on 45 samples to investigate microbe-host interactions. We identified Parvimonas micra (P. micra), an anaerobic oral-derived bacterium, as significantly enriched in tumor tissues and associated with poor prognosis. Moreover, the abundance of P. micra correlated with increased regulatory T cell (Treg cell) infiltration in the ESCC tumor microenvironment. Through cellular and animal experiments, we demonstrate that P. micra promotes tumor growth by secreting p-cresol, a metabolite of amino acid fermentation, which elevates reactive oxygen species levels and induces FOXP3+ Treg differentiation, thereby fostering immunosuppression and tumor growth. Our study establishes a mechanistic link between intratumoral microbiota and the immune microenvironment, highlighting the microbial contribution to ESCC progression and prognosis. Intratumoral Parvimonas micra promotes esophageal cancer via p-cresol–mediated Treg differentiation and immunosuppression.
Science Advances , article en libre accès, 2026