Abstract

Purpose: Recent research has investigated the role of E2F8 in cancer progression. However, whether the progression of ovarian cancer involves E2F8 remains to be elucidated. In this study, the bio-functional consequences of E2F8 knockdown in vitro and in vivo were explored. Experimental Design: E2F8 expression was compared between ovarian cancer and non-cancer tissues, and the association between E2F8 expression and progression-free survival in ovarian cancer patients was analyzed. To demonstrate the function of E2F8 in cell proliferation, migration, and invasion, RNA interference was employed to suppress E2F8 expression in ovarian cancer cell lines. Finally, the effect of E2F8-knockdown was investigated in an ovarian cancer xenograft mouse model. Results: Ovarian cancer tissue exhibited significantly higher E2F8 expression than normal ovarian tissue. Clinical data confirmed that E2F8 was a significant predictor of progression-free survival, and ovarian cancer patients with high E2F8 expression exhibited poorer prognosis than patients with low E2F8 expression. In vitro experiments using E2F8-knockdown ovarian cancer cell lines showed that E2F8 knockdown inhibited cell proliferation, migration, and tumor invasion. Additionally, E2F8 was a potent inducer and modulator of the expression of epithelial-mesenchymal transition (EMT) and Notch signaling pathway-related markers. We confirmed the function of E2F8 in vivo, demonstrating that E2F8-knockdown was significantly correlated with reduced tumor size and weight. Conclusions: In conclusion, our study suggests that E2F8 is highly correlated with ovarian cancer progression; hence, E2F8 may be a prognostic marker and therapeutic target for ovarian malignancy. Note: This abstract was not presented at the meeting. Citation Format: Kyung Jin Eoh, Jong Woo Lee, Young Tae Kim, Peter Jaseok Koo. E2F8 induces proliferation and invasion through the epithelial-mesenchymal transition and notch signaling pathways in ovarian cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 346.

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