Abstract
The underlying causes of breast cancer are diverse, however, there is a striking association between type 2 diabetes and poor patient outcomes. Platelet activation is a common feature of both type 2 diabetes and breast cancer and has been implicated in tumourigenesis through a multitude of pathways. Here transcriptomic analysis of type 2 diabetes patient-derived platelet microvesicles revealed an altered miRNA signature compared with normoglycaemic control patients. Interestingly, interrogation of these data identifies a shift towards an oncogenic signature in type 2 diabetes-derived platelet microvesicles, with increased levels of miRNAs implicated in breast cancer progression and poor prognosis. Functional studies demonstrate that platelet microvesicles isolated from type 2 diabetes patient blood are internalised by triple-negative breast cancer cells in vitro, and that co-incubation with type 2 diabetes patient-derived platelet microvesicles led to significantly increased expression of epithelial to mesenchymal transition markers and triple-negative breast cancer cell invasion compared with platelet microvesicles from healthy volunteers. Together, these data suggest that circulating PMVs in type 2 diabetes patients may contribute to the progression of triple-negative breast cancer.
| Original language | English |
|---|---|
| Article number | e0304870 |
| Number of pages | 20 |
| Journal | PloS ONE |
| Volume | 19 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - 20 Jun 2024 |
Data Availability Statement
The datasets generated during and/or analysed during the current study are available in the GEO repository under accession GSE249475 (https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE249475).
Access to Document
- Tutuianu_etal_PLOSO_Platelet_Derived_Microvesicles_VOR
This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.