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).Funding
This work was funded by a Breast Cancer NOW studentship award to JRB (BCN-2016NovPhD851). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
| Funders | Funder number |
|---|---|
| Breast Cancer NOW | BCN-2016NovPhD851 |