Abstract
Polo-like kinase 1 (PLK1), one of serine/threonine-protein kinase, has been demonstrated to play pivotal roles in malignant transformation. Here we illustrated the clinicopathological significance of PLK1 expression in hepatocellular carcinoma (HCC) in more detail. Immunohistochemistry was performed to detect the expression of PLK1 in 67 HCC patients as well as corresponding noncancerous liver tissues. In addition, the correlation of PLK1 expression with clinicopathological factors or prognosis of HCC was analyzed. Results showed that the expression of PLK1 was increased significantly in HCC tissues than that of corresponding normal liver tissues. The correlation between PLK1 and HCC cell differentiation or capsule invasion was also revealed. We found that PLK1 inhibition promoted cell arrest in G2/M phase of cell cycle and cell apoptosis. Our results also indicated that the potential mechanisms of PLK1 inhibition regulating cell growth involved enhancing expression of caspase3, caspase8, and Bax and decreasing expression of Bcl-2. Furthermore, we also found that PLK1 downregulation inducing inhibition of cell growth was associated with enhancing expression of p53. Thus, we presume that the status of PLK1 expression might be an independent prognostic factor for HCC and targeting PLK1 might be a useful strategy for diagnosis and treatment of human HCC.
Highlights
Cancer is a complicated disease that develops slowly due to gradual accumulation of genetic and epigenetic alterations over time [1, 2]
We found that Polo-like kinase 1 (PLK1) expression has no correlation with patient age, clinical stages, tumor nodules, tumor diameter, lymphatic metastasis, extrahepatic metastasis, with or without tumor thrombi in portal vein, hepatitis B virus (HBV) positive, hepatitis C virus (HCV) positive, and Child-Turcotte grading system for liver function evaluation
We presume that PLK1 is associated with hepatocellular carcinoma (HCC) development
Summary
Cancer is a complicated disease that develops slowly due to gradual accumulation of genetic and epigenetic alterations over time [1, 2]. Tumor cells often harbor mutations followed by activated oncogene expression and inactivated tumorsuppressor expression. These alterations combined with dysregulation of cell division, one of the hallmarks of the cancer phenotype [1]. In spite of the universal property of tumors, many important issues remain to be illustrated, including whether the order of the unsuccessive alterations is critical to cellular malformation and how mutations of cancer pathways are involved in the development of cancer disease. The expression of PLK1 is increased in many types of tumor, including cancer in brain, breast, colon, head and neck, lung, pancreas, bile duct, bladder, and prostate as well as hepatocellular carcinoma (HCC). The inhibition of PLK1 leads to a failure to complete mitosis, eventually resulting in cell death [8]. PLK1 expression shows a close relationship with cancer development and its small molecule inhibitors have been used in clinical trials in advanced cancer patients
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