This study reveals bacterial infection impacts ovarian cancer progression by altering extracellular vesicles, suggesting new therapeutic targets.
Ovarian cancer (OC) is diagnosed at an advanced stage, contributing to its high mortality rate. The presence of concurrent bacterial infections in these patients is a common clinical observation, and the mechanisms by which this coinfection influences tumor progression, still not fully understood. This study investigates the role of extracellular vesicles polydispersity (EVPs) secreted by OC cells in response to bacterial components, aiming to elucidate a potential communication pathway between the OC and the bacterial microenvironment. We stimulated a human OC cell line in vitro with a fraction of E. coli. Our results show that this bacterial stimulation significantly increases the secretion of PEVs by the cancer cells. A subsequent proteomic analysis of these PEVs revealed an enrichment of proteins, including filamin A-B, alpha-enolase, heat shock cognate 71 kDa protein, etc. In addition, the EVPs displayed protease (on fibronectin and gelatin) and phosphatase activity against para-nitrophenyl phosphate, indicating their capacity to alter cellular signaling. This represents a novel mechanism through which bacterial coinfection may influence the biological behavior of OC, potentially contributing to their aggressiveness and the challenges associated with their treatment. Our work highlights the importance of studying the interplay between the tumor and its associated microbiota to better understand ovarian cancer progression and identify new therapeutic targets.
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Sierra-López et al. (2025) studied this question.
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