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Metallothionein 1M suppresses tumorigenesis in hepatocellular carcinoma

Members of the metallothionein (MT) family are involved in metal detoxifcation and in the protection of cells against certain electrophilic carcinogens. In present study, it was found that MT1M was downregulated in more than 77.1% (91/118) of hepatocellular carcinoma (HCC) tissues compared with adja...

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Autores principales: Fu, Cheng-Lin, Pan, Bing, Pan, Ju-Hua, Gan, Mei-Fu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5464848/
https://www.ncbi.nlm.nih.gov/pubmed/28380433
http://dx.doi.org/10.18632/oncotarget.16521
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author Fu, Cheng-Lin
Pan, Bing
Pan, Ju-Hua
Gan, Mei-Fu
author_facet Fu, Cheng-Lin
Pan, Bing
Pan, Ju-Hua
Gan, Mei-Fu
author_sort Fu, Cheng-Lin
collection PubMed
description Members of the metallothionein (MT) family are involved in metal detoxifcation and in the protection of cells against certain electrophilic carcinogens. In present study, it was found that MT1M was downregulated in more than 77.1% (91/118) of hepatocellular carcinoma (HCC) tissues compared with adjacent non-tumor tissues. Furthermore, overexpression of MT1M inhibited cell viability, colony formation, cell migration and invasion in HCC cell lines and tumor cell growth in xenograft nude mice, and activated cell apoptosis in HCC cell lines. In addition, immunohistochemistry analysis showed MT1M was negative or weak staining in tumor tissues but moderate or strong staining in adjacent non-tumor tissues. The sensitivity and specificity of MT1M for HCC diagnosis were 76.27% and 89.83%, respectively. In conclusion, MT1M was identified as a potential tumor marker for HCC and may serve as a useful therapeutic agent for HCC gene therapy.
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spelling pubmed-54648482017-06-21 Metallothionein 1M suppresses tumorigenesis in hepatocellular carcinoma Fu, Cheng-Lin Pan, Bing Pan, Ju-Hua Gan, Mei-Fu Oncotarget Research Paper Members of the metallothionein (MT) family are involved in metal detoxifcation and in the protection of cells against certain electrophilic carcinogens. In present study, it was found that MT1M was downregulated in more than 77.1% (91/118) of hepatocellular carcinoma (HCC) tissues compared with adjacent non-tumor tissues. Furthermore, overexpression of MT1M inhibited cell viability, colony formation, cell migration and invasion in HCC cell lines and tumor cell growth in xenograft nude mice, and activated cell apoptosis in HCC cell lines. In addition, immunohistochemistry analysis showed MT1M was negative or weak staining in tumor tissues but moderate or strong staining in adjacent non-tumor tissues. The sensitivity and specificity of MT1M for HCC diagnosis were 76.27% and 89.83%, respectively. In conclusion, MT1M was identified as a potential tumor marker for HCC and may serve as a useful therapeutic agent for HCC gene therapy. Impact Journals LLC 2017-03-23 /pmc/articles/PMC5464848/ /pubmed/28380433 http://dx.doi.org/10.18632/oncotarget.16521 Text en Copyright: © 2017 Fu et al. http://creativecommons.org/licenses/by/3.0/ This article is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) (CC-BY), which permits unrestricted use and redistribution provided that the original author and source are credited.
spellingShingle Research Paper
Fu, Cheng-Lin
Pan, Bing
Pan, Ju-Hua
Gan, Mei-Fu
Metallothionein 1M suppresses tumorigenesis in hepatocellular carcinoma
title Metallothionein 1M suppresses tumorigenesis in hepatocellular carcinoma
title_full Metallothionein 1M suppresses tumorigenesis in hepatocellular carcinoma
title_fullStr Metallothionein 1M suppresses tumorigenesis in hepatocellular carcinoma
title_full_unstemmed Metallothionein 1M suppresses tumorigenesis in hepatocellular carcinoma
title_short Metallothionein 1M suppresses tumorigenesis in hepatocellular carcinoma
title_sort metallothionein 1m suppresses tumorigenesis in hepatocellular carcinoma
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5464848/
https://www.ncbi.nlm.nih.gov/pubmed/28380433
http://dx.doi.org/10.18632/oncotarget.16521
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