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Low expression of spindle checkpoint protein, Cenp-E, causes numerical chromosomal abnormalities in HepG-2 human hepatoma cells

The aim of the present study was to investigate the expression, localization and role of centromere-associated protein E (Cenp-E) in hepatoma cells. The Cenp-E mRNA expression levels in the HepG-2 human hepatocellular carcinoma and LO2 normal hepatic cell lines following treatment with nocodazole we...

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Autores principales: LIU, BIN, LUO, HONGMEI, WU, GUANG, LIU, JING, PAN, JIE, LIU, ZHUORAN
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4665365/
https://www.ncbi.nlm.nih.gov/pubmed/26722229
http://dx.doi.org/10.3892/ol.2015.3721
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author LIU, BIN
LUO, HONGMEI
WU, GUANG
LIU, JING
PAN, JIE
LIU, ZHUORAN
author_facet LIU, BIN
LUO, HONGMEI
WU, GUANG
LIU, JING
PAN, JIE
LIU, ZHUORAN
author_sort LIU, BIN
collection PubMed
description The aim of the present study was to investigate the expression, localization and role of centromere-associated protein E (Cenp-E) in hepatoma cells. The Cenp-E mRNA expression levels in the HepG-2 human hepatocellular carcinoma and LO2 normal hepatic cell lines following treatment with nocodazole were detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Furthermore, the localization and expression of Cenp-E protein in the two cell types was visualized using indirect immunofluorescence. RT-qPCR was also performed to detect the Cenp-E mRNA expression levels in LO2 cells before and after RNA interference. Additional evaluation of the function of interfered cells was performed using indirect immunofluorescence. The results of RT-qPCR demonstrated that the protein expression levels of Cenp-E in the two cell lines prior to treatment with nocodazole were not significantly different (P>0.05). However, the upregulation of Cenp-E expression levels in the LO2 cells was significantly higher compared with that in the HepG-2 cells during cell division (P<0.05). Indirect immunofluorescence analysis indicated that the Cenp-E protein was predominantly located in the nucleus, and that Cenp-E protein expression in nuclei with abnormal mitosis was markedly lower compared with that in nuclei exhibiting normal mitosis. Indirect immunofluorescence also determined that the ratio of dyskaryosis was significantly higher in cells that had undergone Cenp-E interference compared with normal cells. Thus, the present study indicated that the low expression of Cenp-E mRNA may be an important reason for numerical chromosomal abnormalities in human hepatoma cells.
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spelling pubmed-46653652015-12-31 Low expression of spindle checkpoint protein, Cenp-E, causes numerical chromosomal abnormalities in HepG-2 human hepatoma cells LIU, BIN LUO, HONGMEI WU, GUANG LIU, JING PAN, JIE LIU, ZHUORAN Oncol Lett Articles The aim of the present study was to investigate the expression, localization and role of centromere-associated protein E (Cenp-E) in hepatoma cells. The Cenp-E mRNA expression levels in the HepG-2 human hepatocellular carcinoma and LO2 normal hepatic cell lines following treatment with nocodazole were detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Furthermore, the localization and expression of Cenp-E protein in the two cell types was visualized using indirect immunofluorescence. RT-qPCR was also performed to detect the Cenp-E mRNA expression levels in LO2 cells before and after RNA interference. Additional evaluation of the function of interfered cells was performed using indirect immunofluorescence. The results of RT-qPCR demonstrated that the protein expression levels of Cenp-E in the two cell lines prior to treatment with nocodazole were not significantly different (P>0.05). However, the upregulation of Cenp-E expression levels in the LO2 cells was significantly higher compared with that in the HepG-2 cells during cell division (P<0.05). Indirect immunofluorescence analysis indicated that the Cenp-E protein was predominantly located in the nucleus, and that Cenp-E protein expression in nuclei with abnormal mitosis was markedly lower compared with that in nuclei exhibiting normal mitosis. Indirect immunofluorescence also determined that the ratio of dyskaryosis was significantly higher in cells that had undergone Cenp-E interference compared with normal cells. Thus, the present study indicated that the low expression of Cenp-E mRNA may be an important reason for numerical chromosomal abnormalities in human hepatoma cells. D.A. Spandidos 2015-11 2015-09-18 /pmc/articles/PMC4665365/ /pubmed/26722229 http://dx.doi.org/10.3892/ol.2015.3721 Text en Copyright: © Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
LIU, BIN
LUO, HONGMEI
WU, GUANG
LIU, JING
PAN, JIE
LIU, ZHUORAN
Low expression of spindle checkpoint protein, Cenp-E, causes numerical chromosomal abnormalities in HepG-2 human hepatoma cells
title Low expression of spindle checkpoint protein, Cenp-E, causes numerical chromosomal abnormalities in HepG-2 human hepatoma cells
title_full Low expression of spindle checkpoint protein, Cenp-E, causes numerical chromosomal abnormalities in HepG-2 human hepatoma cells
title_fullStr Low expression of spindle checkpoint protein, Cenp-E, causes numerical chromosomal abnormalities in HepG-2 human hepatoma cells
title_full_unstemmed Low expression of spindle checkpoint protein, Cenp-E, causes numerical chromosomal abnormalities in HepG-2 human hepatoma cells
title_short Low expression of spindle checkpoint protein, Cenp-E, causes numerical chromosomal abnormalities in HepG-2 human hepatoma cells
title_sort low expression of spindle checkpoint protein, cenp-e, causes numerical chromosomal abnormalities in hepg-2 human hepatoma cells
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4665365/
https://www.ncbi.nlm.nih.gov/pubmed/26722229
http://dx.doi.org/10.3892/ol.2015.3721
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