ArticleMicrobial biotechnology2026
Malassezia restricta-Derived Extracellular Vesicles Drive Ovarian Cancer Progression Through JAK2/STAT3-Mediated M2 Macrophage Polarisation.
Article in Microbial biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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8 authors.
Funding
Abstract
The intratumoural mycobiome is a critical constituent of the tumour microenvironment; however, its specific impact on epithelial ovarian cancer (EOC) progression and the underlying molecular mechanisms remain largely elusive. In this study, internal transcribed spacer 1 (ITS1) sequencing revealed a significant enrichment of Malassezia in EOC tissues compared with epithelial borderline ovarian tumours, with its abundance positively correlated with disease progression. Subsequent intratumoural microbiota transplantation and mono-colonisation in a murine EOC model demonstrated that Malassezia restricta substantially accelerated tumour growth and increased M2 macrophage infiltration. Furthermore, in vitro assays established that M. restricta-derived extracellular vesicles (MrEVs) play a pivotal role in inducing M2 macrophage polarisation. Mechanistically, both in vitro and in vivo data showed that MrEVs activate the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signalling pathway, thereby driving M2 polarisation and tumour malignancy. Collectively, these findings identify M. restricta as a pro-tumourigenic fungus in EOC and uncover a previously unrecognised fungal-immune axis that promotes tumour progression. This study provides new insight into the oncogenic role of tumour-resident fungi and highlights the M. restricta EV-JAK2/STAT3 axis as a potential therapeutic target for immune modulation.
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