CENP-H expression was higher in tongue cancer cell lines and nasopharyngeal carcinoma cell lines [20, 21]Therefore, to study centromere proteins may contributes to exploring

the mechanism of chromosome segregation, revealing the mechanism of malignant cellular proliferation and finding cancer marker proteins, and also may provide new targets for carcinoma therapy and prognosis estimation of cancer patients. Reduced expression of CENP-E in human hepatocellular carcinoma CENP-E is also one of the components directly responsible for capturing and stabilizing spindle microtubules by kinetochores [9, 10]. CENP-E interacts with BubR1 and stimulates its kinase activity, which implicates click here its role in activating and maintaining mitotic checkpoint signalling [6, 19]. Deletion CENP-E by various methods could impair the function of spindle checkpoint [9, 12]. In this study we found TSA HDAC chemical structure that the mRNA and protein expression levels of CENP-E were reduced both in HCC tissues and in human hepatocellular carcinoma-derived cell lines (HepG2), and that the LO2 cells transfected with shRNA vector had a decreased

proliferation rate and an increased proportion of aneuploid and apoptosis cells. Reduced expression of CENP-E may be involved in human hepatocarcinogenesis Our evidence presents that the level of CENP-E protein was reduced in the HCC tissues, which implicates that CENP-E may be involved in human hepatocarcinogenesis. We draw this conclusion from two aspects as follows: (1) Aneuploidy is related with tumorigenesis. A majority of human cancer cells are aneuploid due to an underlying chromosomal instability phenotype [22]. Theodor Boveri proposed an aneuploid hypothesis, in which, aneuploid was presumed as a direct cause of cancerous transformation [23]. With the discovery of oncogenes and tumour suppressors in the late 1970s and 1980s, some researchers suggested that heterozygosity

loss might result in the phenotypic expression of mutated tumour suppressor genes in the aneuploid cell, and aneuploid cells may show chromosome polysomy that harbours oncogenes [24]. Aneuploid is still an important cause of tumorigenesis, and oncogenes hypothesis also supports this SPTLC1 point, although there is no direct evidence to confirm that aneuploidy is a primary contributor to tumorigenesis up to now.   (2) Cancer is associated with weakened spindle checkpoint. A growing body of evidence suggests that defects in the spindle checkpoint might promote aneuploidy and tumorigenesis. Mouse with reduced expression of spindle checkpoint proteins survived but developed aneuploidy at an elevated rate, and in some, but not all cases, these animals are more susceptible to spontaneous tumours [25, 26] Cells over-expressing Mad2 developed a large number of chromosome breaks, fragments, and fusions in addition to whole chromosomal aneuploidy [27].