Background <p>Ovarian cancer (OC) is one of the leading causes of cancer related deaths among women. Chemo resistance and distant metastasis are the main reasons of poor prognosis in these patients. Therefore, it is required to assess the molecular mechanisms associated with tumor cell migration and drug resistance. Epithelial mesenchymal transition (EMT) has a key role in OC progression and chemo resistance that can be modulated by various signaling pathways. KCTD12 as a component of K+ channel regulates the EMT process through modulation of signaling pathways. Therefore, we assessed the role of KCTD12 in cell migration and drug response through signaling pathways in ovarian tumor cells.</p> Materials and methods <p>KCTD12 ectopic expression was performed in A2780 cells. Then, we assessed the WNT, NOTCH, and EMT gene expression profiles in KCTD12 overexpressed cells in comparison with non-transfected (control) cells. Cell migration and MTT assays were performed to evaluate the role of KCTD12 in ovarian tumor aggressiveness and cisplatin (CDDP) response.</p> Results <p>KCTD12 induced WNT and NOTCH pathways and EMT process in A2780 cells. It also significantly promoted ovarian tumor cell migration (<i>p</i> = 0.04). Moreover, CDDP resistance was significantly increased following the KCTD12 ectopic expression in A2780 cells (<i>p</i> &lt; 0.0001).</p> Conclusions <p>KCTD12 played as an oncogene and induced CDDP resistance, EMT process, and cell migration via promotion of WNT and NOTCH pathways in OC cells.</p>