Proteomic alterations in extracellular vesicles induced by oncogenic PIK3CA mutations
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Updated: Sep 20, 2025

Direct Stochastic Optical Reconstruction Microscopy of Extracellular Vesicles in Three Dimensions
Published on: August 26, 2021
Mayank Saraswat1,2,3, Kishore Garapati1,2,3, Jinyong Kim1
1Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota, USA.
Abstract:
PIK3CA is one of the most frequently mutated genes in human cancers, with the two most prevalent activating mutations being E545K and H1047R. Although the altered intracellular signaling pathways in these cells have been described, the effect of these mutations on their extracellular vesicles (EVs) has not yet been reported. To study altered cellular physiology and intercellular communication through proteomic analysis of EVs, MCF10A cells and their isogenic mutant versions (PIK3CA E545K and H1047R) were cultured and their EVs enriched by differential ultracentrifugation. Proteins were extracted, digested with trypsin and the peptides labeled with tandem mass tag (TMT) reagents and analyzed by liquid chromatography tandem mass spectrometry (LC-MS/MS). Four thousand six hundred and fifty-five peptides were identified from 579 proteins of which 522 proteins have been previously described in EVs. Relative quantitation revealed altered levels of EV proteins including several cell adhesion molecules. Mesothelin, E-cadherin, and epithelial cell adhesion molecule were elevated in both mutant cell-derived EVs. Markers of tumor invasion and progression like galectin-3 and transforming growth factor beta induced protein were increased in both mutants. Overall, activating mutations in PIK3CA result in altered EV composition with characteristic changes associated with these hotspot mutations.
Insights
Activating mutations in the PIK3CA gene alter the protein composition of extracellular vesicles (EVs). These changes include elevated cell adhesion molecules and markers of tumor invasion, impacting intercellular communication in cancer.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- PIK3CA is frequently mutated in human cancers, with E545K and H1047R being common activating mutations.
- Intracellular signaling pathways affected by these mutations are known, but their impact on extracellular vesicles (EVs) is uncharacterized.
Purpose of the Study:
- To investigate the proteomic changes in EVs derived from cells with PIK3CA activating mutations.
- To understand how these mutations affect intercellular communication via EVs.
Main Methods:
- MCF10A cells and isogenic mutants (PIK3CA E545K, H1047R) were cultured.
- EVs were isolated using differential ultracentrifugation.
- Proteomic analysis was performed using tandem mass tag (TMT) labeling and liquid chromatography tandem mass spectrometry (LC-MS/MS).
Main Results:
- 579 proteins were identified in EVs, with 522 previously described.
- EVs from both mutant cell lines showed elevated levels of cell adhesion molecules (Mesothelin, E-cadherin, EpCAM).
- Markers associated with tumor invasion and progression (Galectin-3, TGFBI) were increased in mutant EVs.
Conclusions:
- Activating PIK3CA mutations lead to significant alterations in EV protein composition.
- These alterations include changes in cell adhesion molecules and tumor progression markers.
- Mutant-derived EVs exhibit characteristic proteomic changes associated with these hotspot mutations.
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