Ovarian cancer is one of most lethal cancer; however the interaction between cancer cells and immune system is not fully understood. Our previous study showed that miR-193a is epigenetically silenced by binding of repressive complex containing E2F6 in ovarian cancer cells. Interestingly, computational and biological experiments found that E2F6 mRNA is a target of miR-193a, we therefore aim to explore how E2F6 involves in anti-tumor immune response. Results from RNA-Seq in CP70 ovarian cancer cells depleted with E2F6, found that PBX1, a transcriptional activator of the immunosuppressive cytokine IL-10, were down-regulated in the knockdown cells as compared with control. Overexpression of E2F6 3’UTR but not miR-193a MRE mutant can upregulate PBX1 and IL-10 in ovarian cancer cells. Importantly, differentiation of THP-1 monocyte into mature dendritic cells can be inhibited by addition of IL-10 or conditional media from cells overexpressing E2F6 3’UTR. Taken together, overexpression of E2F6 3’UTR can inhibit the differentiation of dendritic cell possibly through ceRNA-mediated mechanism thus suppressing the anti-tumor immune response in ovarian cancer.