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      Suppression of KIF3B Expression Inhibits Human Hepatocellular Carcinoma Proliferation

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          Abstract

          Background

          Human hepatocellular carcinoma (HCC) is one of the most common fatal cancers and an important health problem worldwide, but its mechanism is still unclear. Microtubule (MT) kinesin motor proteins orchestrate a variety of cellular processes (e.g. mitosis, motility and organelle transportation) and have been involved in human carcinogenesis. KIF3B, the kinesin superfamily of proteins (KIFs), plays an important role in the regulation of mitotic progression.

          Aim

          The expression of KIF3B and its involvement in HCC was investigated.

          Methods

          Western blot and immunohistochemistry were used to measure the expression of KIF3B protein in HCC and adjacent non-tumorous tissues in 57 patients and Cell Counting Kit-8 to analyze the effects of growth and interference of KIF3B in the cell cycle process.

          Results

          KIF3B protein level was increased in HCC tissues compared with the adjacent non-tumorous tissues. It was significantly associated with histological differentiation, tumor size, the level of alpha fetal protein (AFP) and proliferation marker Ki-67. Over-expression of KIF3B was correlated with poor survival. Following release of HepG2 cells from serum starvation, the expression of KIF3B was up-regulated. Furthermore, suppression of KIF3B not only decreased cancer cell growth but also induced apoptosis of cells.

          Conclusions

          Our results suggested that KIF3B expression was upregulated in HCC tumor tissues and proliferating HCC cells, and an increased KIF3B expression was associated with poor overall survival. KIF3B over-expression is involved in the pathogenesis of hepatocellular carcinoma and may serve as a potential therapeutic target for human HCC.

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          Rising incidence of hepatocellular carcinoma in the United States.

          H B El-Serag, A Mason (1999)
          Clinical observations have suggested that the number of cases of hepatocellular carcinoma has increased in the United States. We analyzed data from the Surveillance, Epidemiology, and End Results (SEER) data base to determine the age-adjusted incidence of hepatocellular carcinoma from 1976 to 1995, data from the U.S. vital-statistics data base to determine age-adjusted mortality rates from 1981 to 1995, and data from the Department of Veterans Affairs to determine age-adjusted rates of hospitalization for the disease from 1983 to 1997. The incidence of histologically proved hepatocellular carcinoma increased from 1.4 per 100,000 population (95 percent confidence interval, 1.3 to 1.4) for the period from 1976 to 1980 to 2.4 per 100,000 (95 percent confidence interval, 2.3 to 2.4) for the period from 1991 to 1995. Among black men, the incidence was 6.1 per 100,000 for the period from 1991 to 1995, and among white men, it was 2.8 per 100,000. There was a 41 percent increase in the mortality rate from primary liver cancer and a 46 percent increase in the proportion of hospitalizations attributable to this disease during the periods studied. The incidence increased significantly among younger persons (40 to 60 years old) during the period from 1991 to 1995 as compared with earlier periods. An increase in the number of cases of hepatocellular carcinoma has occurred in the United States over the past two decades. The age-specific incidence of this cancer has progressively shifted toward younger people.
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            Analysis of the kinesin superfamily: insights into structure and function.

            Harukata Miki, Yasushi Okada, Nobutaka Hirokawa (2005)
            Kinesin superfamily proteins (KIFs) are key players or 'hub' proteins in the intracellular transport system, which is essential for cellular function and morphology. The KIF superfamily is also the first large protein family in mammals whose constituents have been completely identified and confirmed both in silico and in vivo. Numerous studies have revealed the structures and functions of individual family members; however, the relationships between members or a perspective of the whole superfamily structure until recently remained elusive. Here, we present a comprehensive summary based on a large, systematic phylogenetic analysis of the kinesin superfamily. All available sequences in public databases, including genomic information from all model organisms, were analyzed to yield the most complete phylogenetic kinesin tree thus far, comprising 14 families. This comprehensive classification builds on the recently proposed standardized nomenclature for kinesins and allows systematic analysis of the structural and functional relationships within the kinesin superfamily.
            Article 0 comments Cited 185 times – based on 0 reviews     Review now
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              p27kip1: a multifunctional cyclin-dependent kinase inhibitor with prognostic significance in human cancers.

              Ricardo V. Lloyd, Lori Erickson, Long Yi Jin … (1999)
              p27kip1 (p27) is a member of the universal cyclin-dependent kinase inhibitor (CDKI) family. p27 expression is regulated by cell contact inhibition and by specific growth factors, such as transforming growth factor (TGF)-beta. Since the cloning of the p27 gene in 1994, a host of other functions have been associated with this cell cycle protein. In addition to its role as a CDKI, p27 is a putative tumor suppressor gene, regulator of drug resistance in solid tumors, and promoter of apoptosis; acts as a safeguard against inflammatory injury; and has a role in cell differentiation. The level of p27 protein expression decreases during tumor development and progression in some epithelial, lymphoid, and endocrine tissues. This decrease occurs mainly at the post-translational level with protein degradation by the ubiquitin-proteasome pathway. A large number of studies have characterized p27 as an independent prognostic factor in various human cancers, including breast, colon, and prostate adenocarcinomas. Here we review the role of p27 in the regulation of the cell cycle and other cell functions and as a diagnostic and prognostic marker in human neoplasms. We also review studies indicating the increasingly important roles of p27, other CDKIs, and cyclins in endocrine cell hyperplasia and tumor development.
              Article 0 comments Cited 76 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Yixin Zhang: Zhangyix0513@163.com
                Tianyi Zhang: pro_zty001@163.com
                Journal
                Journal ID (nlm-ta): Dig Dis Sci
                Journal ID (iso-abbrev): Dig. Dis. Sci
                Title: Digestive Diseases and Sciences
                Publisher: Springer US (Boston )
                ISSN (Print): 0163-2116
                ISSN (Electronic): 1573-2568
                Publication date (Electronic): 25 December 2013
                Publication date PMC-release: 25 December 2013
                Publication date (Print): 2014
                Volume: 59
                Pages: 795-806
                Affiliations
                [ ]Key Laboratory of Neuroregeneration, Nantong University, Nantong, 226001 Jiangsum People’s Republic of China
                [ ]Department of Pathology, Nantong University Cancer Hospital, Nantong, 226001 Jiangsu People’s Republic of China
                [ ]Department of Nutrition, Nantong University Hospital, Nantong, 226001 Jiangsu People’s Republic of China
                Article
                Publisher ID: 2969
                DOI: 10.1007/s10620-013-2969-2
                PMC ID: 3958719
                PubMed ID: 24368420
                SO-VID: c0d948a8-2b07-4a06-a549-0fd85cdfea6a
                Copyright © © The Author(s) 2013
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.

                History
                Date received : 21 May 2013
                Date accepted : 15 November 2013
                Categories
                Subject: Original Article
                Custom metadata
                issue-copyright-statement © Springer Science+Business Media New York 2014

                ScienceOpen disciplines: Gastroenterology & Hepatology
                Keywords: human hepatocellular carcinoma (hcc),kif3b,cell proliferation,pathogenesis
                Data availability:
                ScienceOpen disciplines: Gastroenterology & Hepatology
                Keywords: human hepatocellular carcinoma (hcc), kif3b, cell proliferation, pathogenesis

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