Serous ovarian tumour is the deadliest of all gynaecologic carcinomas. The advanced stage of the disease and the development of drug resistance are main reasons for unsuccesful therapy. While searching for a common marker(s) responsible for regulating molecular mechanisms of drug resistance and the occurrence of epithelial-mesenchymal transition (EMT), gene expression analysis of ovarian tumour cell lines, parental MES-OV and carboplatin (CBP) resistant MES-OV 8CBP by microarray assay was performed previously as part of preliminary research. Among others, the increased expression of gene DNER that encodes DNER protein, an alternative activator of Notch signalling pathway, was found. This work sought to determine whether DNER plays a role in the CBP resistance of OVCAR-3 7CBP GFP cells and in the development of a mesenchymal-like phenotype. The OVCAR-3 7CBP GFP cell line has been shown to be 2-3 times more resistant to CBP than the parent OVCAR-3 GFP cell line and has increased expression of mesenchymal-like phenotype and decreased expression of the epithelial-like phenotype markers. The RT-qPCR method confirmed the result of preliminary studies on increased DNER expression in the MES-OV 8CBP cell line relative to the parent cells, as well as in two additional human ovarian cancer cell lines resistant to CBP, OVCAR-3 7CBP GFP and SK-OV-3 6CBP. The importance of DNER in response to CBP was observed after short-term exposure of OVCAR-3 GFP and OVCAR-3 7CBP GFP to a clinical dose of CBP when DNER expression was increased only in the resistant cell line. At the moment the lack of specific anti-DNER antibody has made it impossible to determine the constitutive expression of DNER protein in experimental cell model and to achived the set goals.