Effect of Cytostatic Drugs on the mRNA Expression Levels of Ribonuclease κ in Breast and Ovarian Cancer Cells
Asimina S. Gkratsou, Emmanuel G. Fragoulis and Diamantis C. Sideris
Affiliation: University of Athens, Faculty of Biology, Department of Biochemistry and Molecular Biology, Panepistimioupolis, 15701, Athens, Greece.
Keywords: BT-20, carboplatin, cisplatin, docetaxel, epirubicin, paclitaxel, RNase κ, SKOV-3, vinorelbine.
Breast and ovarian cancers remain a major public health issue, constituting a major cause of female morbidity and mortality
worldwide. Even though systemic chemotherapy remains the main course of action for both types of cancer, current research studies aim
at the discovery of novel therapeutic targets. Ribonucleases, due to their apparent implication in gene expression regulation, may serve as
potential anticancer drugs. Human RNase κ is an endoribonuclease belonging in a recently identified family of proteins. Recent data from
expression microarray studies reveal that the RNase κ gene is found either up- or downregulated in a number of human cancers,
indicating a possible diagnostic and/or prognostic utility.The aim of this study was to investigate modulations in the expression levels of
RNase κ gene, in breast and ovarian cancer cells, as a response to treatment with different chemotherapeutic agents. BT-20 breast cancer
cells and SKOV-3 ovarian cancer cells were treated with the cytotoxic drugs paclitaxel, docetaxel, cisplatin, carboplatin, epirubicin and
vinorelbine. Gene expression analysis was performed by the comparative CT method also known as 2–ΔΔCT method. The results revealed a
distinct increase in the expression levels of RNase κ mRNA (up to 9-fold) after treatment with the antineoplastic agent paclitaxel in both
cell lines, while treatment with the remaining anticancer drugs did not alter drastically the mRNA levels of RNase κ. Based on the fact
that paclitaxel exerts its cytotoxic action by inducing apoptosis, the results could be indicative of a potential implication of RNase κ in apoptosis-related pathways.
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