Introduction
High grade serous ovarian cancer (HGSOC) is the most lethal gynecological cancer and is often diagnosed at later stages when current therapies are no longer effective. One alternative therapeutic strategy being investigated is the regulation of microRNAs in ovarian cancer. The miR-200 family of microRNAs has been heavily implicated in the negative regulation of epithelial to mesenchymal transition (EMT) and metastasis. Our previous work on breast cancer  showed that miR-200s are potent inhibitors of cancer growth and metastasis. Therefore, the goal of this research was to determine whether miR-200s have similar effects in ovarian cancer.

Methods
Murine HGSOC cell lines ID8 and 28-2 were infected with lentiviral vectors to stably overexpress all 5 members of the miR-200 family. qPCR confirmed miR-200 overexpression and was used to evaluate the expression of EMT genes. Matrigel coated transwell assays were used to assess invasion while Annexin-V flow cytometry was used to assess apoptosis and BrdU flow cytometry was used to assess proliferation. RNA sequencing was performed to identify differentially expressed genes. 

Results
miR-200 overexpressing cell lines exhibited decreased mesenchymal gene expression, decreased invasion and proliferation, and increased apoptosis. RNA sequencing data showed that there were 291 shared genes that were differentially expressed in both miR-200 overexpressing cell lines compared to their controls. Analysis of these genes showed that miR-200s may modulate migration and EMT.

Conclusions
We found that overexpressing miR-200s in two different murine HGSOC cell lines decreased properties that are crucial to the progression of ovarian cancer. These preliminary findings on miR-200s warrant future studies in vivo as they may prove to be an effective therapy for ovarian cancer.