Abstract Introduction: Epithelial to mesenchymal transition (EMT) is an important process during cancer progression by which epithelial cells acquire mesenchymal phenotype and show reduced intercellular adhesion as well as increased motility. Interfering PI3K/AKT pathway has been considered an anti-EMT target therapy, due to its effect in restoration of E-cadherin function and inhibition of transcription factors that repress the E-cadherin promoter, such as Snail, Slug, and Twist. Aim: Investigate the antitumor effects of treatment with PI3K/mTOR dual inhibitor, NVP-BEZ235, in biological behavior of lymph node metastatic vulva cancer cell line (SW962), as a potential anti-EMT agent in vulvar tumor. Methods: we performed in vitro assays and evaluated the expression of proteins related to PI3K/Akt/mTOR pathway as well as Vimentin and E-cadherin, relevant EMT biomarkers. All results were presented as mean standard deviation and were compared using the unpaired t test or ANOVA followed by the Bonferroni post test using Graph Pad InStat v3.02 software. P values < 0.05 were considered statistically significant. Results: Treatment with NVP-BEZ235 resulted in a significant decrease in cell migration (p< 0.001), proliferation (p< 0.01) and invasion (p<0.05). The phosphorylation of AKT, S6K, 4E-BP1 and p70S6 was markedly reduced by NVP-BEZ235 treatment. In contrast, the levels of p-GSK3β (Ser9) were increased. Our qualitative results demonstrated that the localization pattern of E-cadherin and Vimentin protein was similar between control and treatment groups. We observed Vimentin protein only in isolated cells and, E-cadherin protein was found exclusively in cell clusters, demonstrating EMT-like events in SW962 cells. The expression of E-cadherin in SW962 cells treated was slightly increased and the levels of Vimentin was reduced in these cells. Conclusion: The present study suggests that NVP-BEZ235 is an effective inhibitor of PI3K/mTOR pathway, resulting in the decrease of Vimentin expression, an important EMT marker, as well as of other essential tumor events, such as proliferation, migration and invasion of vulva cancer. Taken together, these findings not only provide a novel insight into the actions of NVP-BEZ235 as inhibitor of EMT process in cancer progression, but also highlight a novel potential therapeutic option for the treatment of aggressive tumors such as vulvar carcinoma. Citation Format: Iara Rodrigues, Bruna Rodrigues, Fernanda Giudice, Glauco Baiocchi, Fernando Augusto Soares, Vilma Martins, Rafael Malagoli Rocha. A dual PI3K/mTOR inhibitor as potential therapeutic option for vulvar cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 2662. doi:10.1158/1538-7445.AM2015-2662