| First Author | Zheng W | Year | 2019 |
| Journal | Cell Rep | Volume | 29 |
| Issue | 7 | Pages | 1747-1755.e4 |
| PubMed ID | 31722193 | Mgi Jnum | J:300062 |
| Mgi Id | MGI:6488997 | Doi | 10.1016/j.celrep.2019.10.016 |
| Citation | Zheng W, et al. (2019) Lung Mammary Metastases but Not Primary Tumors Induce Accumulation of Atypical Large Platelets and Their Chemokine Expression. Cell Rep 29(7):1747-1755.e4 |
| abstractText | The tumor microenvironment (TME) at the metastatic site consists of multiple components with considerable cellular heterogeneity. To test whether endothelial cells (ECs) associated with lung metastases express a distinct gene expression program that promotes metastatic growth, we isolated CD31(+)/CD45(-) cells from lung mammary cancer metastases for RNA sequencing and found CD44 upregulation. Unexpectedly, the CD44(+) subset did not comprise authentic ECs nor were they bone-marrow-derived CD45(-) endothelial progenitor cells. Instead, they were a population of large platelets that are distinct from regular small platelets. These CD44(+) large platelets were enriched in lung metastases but not primary mammary tumors and upregulated myeloid cell-regulating chemokines indicative of potential regulation of metastasis via indirect mechanisms. Identification of this cellular player in the TME of metastasis suggests a role for the recently identified lung-resident megakaryocytes (MKs) and offers an unexplored route to discover novel mechanisms and an opportunity for therapeutic interventions. |
