Abstract:
:Uterine carcinosarcomas (UCSs) are highly aggressive malignancies associated with poor prognoses and limited treatment options. These tumors are hypothesized to develop from the endometrial adenocarcinoma (EAC) through epithelial-mesenchymal transition (EMT). We test this long-standing hypothesis by depleting miR-200, a family of microRNAs critical for EMT, in EAC cell lines. Our data suggest that UCSs do not develop from EACs via EMT. Clinically more relevant, we show that miR-200 expression in UCS cells induces a robust mesenchymal-epithelial transition (MET). Using in vitro and murine xenograft models, we demonstrate decreased growth and aggressiveness of miR-200-overexpressing UCS cell lines. Whole transcriptome analysis confirmed changes consistent with an MET and also revealed changes in angiogenic genes expression. Finally, by treatment of UCS-xenografted mice with miR-200c incorporated in DOPC nanoliposomes, we demonstrate anti-tumor activities. These findings suggest that ectopic miR-200 expression using advanced microRNA therapeutics may be a potential treatment approach for patients with UCS.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Tseng JH,Bisogna M,Hoang LN,Olvera N,Rodriguez-Aguayo C,Lopez-Berestein G,Sood AK,Levine DA,Jelinic Pdoi
10.1038/s41598-017-03972-7subject
Has Abstractpub_date
2017-06-15 00:00:00pages
3614issue
1issn
2045-2322pii
10.1038/s41598-017-03972-7journal_volume
7pub_type
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