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Malic enzyme 1 (ME1) is a potential oncogene in gastric cancer cells and is associated with poor survival of gastric cancer patients

BACKGROUND AND OBJECTIVE: Gastric cancer is one of the most common cancers worldwide. However, the mechanisms associated with this disease are still not clear. Malic enzyme 1 (ME1) is a metabolic enzyme that is overexpressed in various cancers. Here, we examined whether it is involved in gastric can...

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Autores principales: Shi, Yanyan, Zhou, Siliang, Wang, Pan, Guo, Yanlei, Xie, Bingteng, Ding, Shigang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6628973/
https://www.ncbi.nlm.nih.gov/pubmed/31371996
http://dx.doi.org/10.2147/OTT.S203228
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author Shi, Yanyan
Zhou, Siliang
Wang, Pan
Guo, Yanlei
Xie, Bingteng
Ding, Shigang
author_facet Shi, Yanyan
Zhou, Siliang
Wang, Pan
Guo, Yanlei
Xie, Bingteng
Ding, Shigang
author_sort Shi, Yanyan
collection PubMed
description BACKGROUND AND OBJECTIVE: Gastric cancer is one of the most common cancers worldwide. However, the mechanisms associated with this disease are still not clear. Malic enzyme 1 (ME1) is a metabolic enzyme that is overexpressed in various cancers. Here, we examined whether it is involved in gastric cancer. METHODS: ME1 expression was knocked down in the gastric cancer cell line SGC7901. Cell growth and migration were measured using a real-time microelectronic cell sensor system. Cell invasion was measured using a Transwell assay. Cell cycle analysis was also performed to examine cell cycle arrest. A gastric cancer tissue microarray of gastric cancer was stained using immunohistochemistry. ME1 expression levels were also statistically analysed. RESULTS: ME1 knockdown in gastric cancer SGC7901 cells significantly inhibited cell proliferation, migration, and invasion. Cell cycle arrest was induced in the G2 phase. Further, ME1 expression was significantly correlated with gastric cancer patient prognosis based on both univariable and multivariable survival analysis. No significant difference was found between ME1 expression in gastric cancer tissues and that in adjacent tissues. CONCLUSION: Our results provide evidence that ME1 is a key factor for gastric cancer. ME1 might be pro-oncogenic during both the development and migration of gastric cancer; it also might be related to gastric cancer patient survival.
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spelling pubmed-66289732019-08-01 Malic enzyme 1 (ME1) is a potential oncogene in gastric cancer cells and is associated with poor survival of gastric cancer patients Shi, Yanyan Zhou, Siliang Wang, Pan Guo, Yanlei Xie, Bingteng Ding, Shigang Onco Targets Ther Original Research BACKGROUND AND OBJECTIVE: Gastric cancer is one of the most common cancers worldwide. However, the mechanisms associated with this disease are still not clear. Malic enzyme 1 (ME1) is a metabolic enzyme that is overexpressed in various cancers. Here, we examined whether it is involved in gastric cancer. METHODS: ME1 expression was knocked down in the gastric cancer cell line SGC7901. Cell growth and migration were measured using a real-time microelectronic cell sensor system. Cell invasion was measured using a Transwell assay. Cell cycle analysis was also performed to examine cell cycle arrest. A gastric cancer tissue microarray of gastric cancer was stained using immunohistochemistry. ME1 expression levels were also statistically analysed. RESULTS: ME1 knockdown in gastric cancer SGC7901 cells significantly inhibited cell proliferation, migration, and invasion. Cell cycle arrest was induced in the G2 phase. Further, ME1 expression was significantly correlated with gastric cancer patient prognosis based on both univariable and multivariable survival analysis. No significant difference was found between ME1 expression in gastric cancer tissues and that in adjacent tissues. CONCLUSION: Our results provide evidence that ME1 is a key factor for gastric cancer. ME1 might be pro-oncogenic during both the development and migration of gastric cancer; it also might be related to gastric cancer patient survival. Dove 2019-07-11 /pmc/articles/PMC6628973/ /pubmed/31371996 http://dx.doi.org/10.2147/OTT.S203228 Text en © 2019 Shi et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Shi, Yanyan
Zhou, Siliang
Wang, Pan
Guo, Yanlei
Xie, Bingteng
Ding, Shigang
Malic enzyme 1 (ME1) is a potential oncogene in gastric cancer cells and is associated with poor survival of gastric cancer patients
title Malic enzyme 1 (ME1) is a potential oncogene in gastric cancer cells and is associated with poor survival of gastric cancer patients
title_full Malic enzyme 1 (ME1) is a potential oncogene in gastric cancer cells and is associated with poor survival of gastric cancer patients
title_fullStr Malic enzyme 1 (ME1) is a potential oncogene in gastric cancer cells and is associated with poor survival of gastric cancer patients
title_full_unstemmed Malic enzyme 1 (ME1) is a potential oncogene in gastric cancer cells and is associated with poor survival of gastric cancer patients
title_short Malic enzyme 1 (ME1) is a potential oncogene in gastric cancer cells and is associated with poor survival of gastric cancer patients
title_sort malic enzyme 1 (me1) is a potential oncogene in gastric cancer cells and is associated with poor survival of gastric cancer patients
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6628973/
https://www.ncbi.nlm.nih.gov/pubmed/31371996
http://dx.doi.org/10.2147/OTT.S203228
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