CSE1L was recently shown to associate with a subset of p53 target promoters, and reduced CSE1L expression decreased 53-mediated transcription and thus lowered apoptosis [31]. Our studies

showed that increased CSE1L expression can enhance doxorubicin-induced p53 accumulation [12, 13]; therefore, CSE1L regulates p53 protein accumulation induced by chemotherapeutic drugs. Other studies of ours also showed that interferon-γ treatment increased CSE1L expression in cancer cells [23] and interferon-γ co-treatment enhanced doxorubicin-induced selleck inhibitor p53 accumulation of Hep G2 hepatoma cells [32]. Thus, interferon-γ may increase doxorubicin-induced p53 accumulation by modulating CSE1L expression. CSE1L is highly expressed in cancer, and FG4592 the results of our studies suggest that CSE1L plays a role in regulating p53 accumulation induced

by chemotherapeutic drugs. Therefore, CSE1L may play an important role in mediating the cytotoxicities of chemotherapeutic drugs against cancer cells in cancer chemotherapy. Also, CSE1L may be a target for developing strategies to improve the efficacy and outcomes of cancer chemotherapy. CSE1L expression in cancer CSE1L is highly expressed in various cancer types, and its expression level is positively correlated with high tumor stage, high tumor grade, and worse outcomes of cancer patients. The CSE1L gene is located on chromosome 20q13, a region frequently harbors amplifications that correlate with cancer aggression [33–35]. The copy number of the CSE1L gene is increased in breast, colon, and bladder cancer cell lines [36]. An array-based comparative genomic Vorinostat hybridization study showed high-frequency amplifications of the CSE1L gene in nasopharyngeal carcinomas [37] and in medulloblastomas [38]. The results of array-based comparative genomic hybridization showed that 57.1% of the glioblastoma multiforme cases had high-frequency amplification of the CSE1L gene [39]. Idbaih et al. investigated a series of 16 low-grade gliomas and their subsequent progression to higher-grade

malignancies using a one-megabase bacterial artificial chromosome (BAC)-based array comparative genomic hybridization technique, and reported PRKACG that the CSE1L gene was associated with the progression of gliomas [40]. The results of another study using microarray-based detection showed that CSE1L was highly expressed in nasopharyngeal carcinomas [41]. Combined cytogenetic, array-based comparative genomic hybridization studies and expression analyses also showed that CSE1L was significantly overexpressed in advanced prostate cancer xenografts [42]. The results of a pathological study showed that expression of CSE1L was not detected in normal hepatocytes, while strong CSE1L expression was detected in hepatocellular carcinoma [10].