# Secretion of Extracellular Microvesicles Induced by a Fraction of Escherichia coli: Possible Role in Ovarian Cancer with Bacterial Coinfections

**Authors:** Francisco Sierra-López, Juan Carlos Fernández-Hernández, Lidia Baylón-Pacheco, Verónica Ivonne Hernández-Ramírez, Juan Carlos Bravata-Alcántara, Vanessa Iglesias-Vázquez, Susana Bernardo-Hernández, Daniel Medrano-Espinosa, Gustavo Acosta-Altamirano, Patricia Talamás-Rohana, José Luis Rosales-Encina, Mónica Sierra-Martínez

PMC · DOI: 10.3390/ijms262110653 · International Journal of Molecular Sciences · 2025-11-01

## TL;DR

This study explores how bacterial infections might influence ovarian cancer by increasing the release of extracellular vesicles that alter cellular signaling.

## Contribution

The study reveals a novel mechanism linking bacterial coinfection and ovarian cancer progression through extracellular vesicle secretion.

## Key findings

- Bacterial stimulation significantly increases extracellular vesicle secretion by ovarian cancer cells.
- Proteomic analysis shows enrichment of specific proteins and enzymatic activities in these vesicles.
- The findings suggest a potential role for these vesicles in altering tumor behavior and treatment challenges.

## Abstract

Ovarian cancer (OC) is usually 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 are still not fully understood. This study investigates the role of polydisperse extracellular vesicles (PEVs) secreted by OC cells in response to bacterial components, aiming to elucidate a potential communication pathway between 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 cancer cells. A subsequent proteomic analysis of these PEVs revealed an enrichment of proteins, including filamin A, filamin B, alpha-enolase, and heat shock cognate 71 kDa protein. In addition, the PEVs displayed protease activity (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 if bacteria interact with tumor cells, 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.

## Linked entities

- **Proteins:** FLNA (filamin A), FLNB (filamin B)
- **Chemicals:** para-nitrophenyl phosphate (PubChem CID 4686862), fibronectin (PubChem CID 13085557)
- **Diseases:** ovarian cancer (MONDO:0005140)
- **Species:** Escherichia coli (taxon 562), Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** FN1 (fibronectin 1) [NCBI Gene 2335] {aka CIG, ED-B, FINC, FN, FNZ, GFND}, FLNB (filamin B) [NCBI Gene 2317] {aka ABP-278, ABP-280, FH1, FLN-B, FLN1L, LRS1}, ENO1 (enolase 1) [NCBI Gene 2023] {aka ENO1-IT1, ENO1L1, HEL-S-17, MPB1, NNE, PPH}, FLNA (filamin A) [NCBI Gene 2316] {aka ABP-280, ABPX, CSBS, CVD1, FGS2, FLN}
- **Diseases:** OC (MESH:D010051), cancer (MESH:D009369), bacterial infections (MESH:D001424)
- **Chemicals:** para-nitrophenyl phosphate (-)
- **Species:** Homo sapiens (human, species) [taxon 9606], Escherichia coli (E. coli, species) [taxon 562]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12608175/full.md

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12608175/full.md

## References

51 references — full list in the complete paper: https://tomesphere.com/paper/PMC12608175/full.md

---
Source: https://tomesphere.com/paper/PMC12608175