C-terminal binding protein (CtBP) was first established as a phosphoprotein bound to the C terminal of the E1A protein [4]. The CtBP family consists of two genes, CtBP1 and CtBP2, which are conserved among both vertebrates and invertebrates [5]. CtBPs reportedly function primarily as transcriptional co-repressors and play important roles in development and tumorigenesis [6–9]. CtBPs have also been demonstrated to function as context-dependent transcriptional activators [10, 11]. A growing body of evidence indicates that CtBP2 is aberrantly upregulated in a variety of cancers and that its expression promotes cancer progression. Zhang et al. reported that CtBP2 was overexpressed in prostate cancer tissues and associated with poor outcome and several indicators of malignancy, including elevated serum PSA levels, advanced tumor stages and higher Gleason scores. Zhang et al. also reported that CtBP2 expression promoted prostate cancer cell proliferation through c-Myc signaling [12]. Barroilhet et al. found that CtBP2 was aberrantly elevated in human ovarian tumors and that CtBP2 expression accelerated tumor cell growth and mobility [13]. Similar findings have also been reported in breast cancer studies that examined CtBP2 expression [14, 15]. However, the mechanism governing CtBP2 overexpression in cancer remains unclear.
