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Higher autocrine motility factor/glucose-6-phosphate isomerase expression is associated with tumorigenesis and poorer prognosis in gastric cancer

BACKGROUND: Glucose-6-phosphate isomerase (GPI) is a glycolytic-related enzyme that inter-converts glucose-6-phosphate and fructose-6-phosphate in the cytoplasm. This protein is also secreted into the extracellular matrix by cancer cells and is, therefore, also called autocrine motility factor (AMF)...

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Autores principales: Ma, Yu-Teng, Xing, Xiao-Fang, Dong, Bin, Cheng, Xiao-Jing, Guo, Ting, Du, Hong, Wen, Xian-Zi, Ji, Jia-Fu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6208529/
https://www.ncbi.nlm.nih.gov/pubmed/30464597
http://dx.doi.org/10.2147/CMAR.S177441
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author Ma, Yu-Teng
Xing, Xiao-Fang
Dong, Bin
Cheng, Xiao-Jing
Guo, Ting
Du, Hong
Wen, Xian-Zi
Ji, Jia-Fu
author_facet Ma, Yu-Teng
Xing, Xiao-Fang
Dong, Bin
Cheng, Xiao-Jing
Guo, Ting
Du, Hong
Wen, Xian-Zi
Ji, Jia-Fu
author_sort Ma, Yu-Teng
collection PubMed
description BACKGROUND: Glucose-6-phosphate isomerase (GPI) is a glycolytic-related enzyme that inter-converts glucose-6-phosphate and fructose-6-phosphate in the cytoplasm. This protein is also secreted into the extracellular matrix by cancer cells and is, therefore, also called autocrine motility factor (AMF). METHODS: To clarify the roles of AMF/GPI in gastric cancer (GC), we collected 335 GC tissues and the corresponding adjacent noncancerous tissues, performed immunohistochemical studies, and analyzed the relationship between AMF/GPI expression and the patients’ clinicopathologic features. RESULTS: AMF/GPI expression was found to be significantly higher in the GC group than in the corresponding noncancerous tissue group (P<0.001). Additionally, AMF/GPI expression positively associated with a higher TNM stage and poorer prognosis in patients. Through Kaplan–Meier analysis and according to the Oncomine database, we found that AMF/GPI was overexpressed in GC tissues compared to normal mucosa, and the patients with higher AMF/GPI expression had poorer outcomes. We used AMF/GPI-silenced GC cell lines to observe how changes in AMP/GPI affect cellular phenotypes. AMF/GPI knockdown suppressed proliferation, migration, invasion, and glycolysis, and induced apoptosis in GC cells. CONCLUSION: These findings suggest that AMF/GPI overexpression is involved in carcinogenesis and promotes the aggressive phenotypes of GC cells.
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spelling pubmed-62085292018-11-21 Higher autocrine motility factor/glucose-6-phosphate isomerase expression is associated with tumorigenesis and poorer prognosis in gastric cancer Ma, Yu-Teng Xing, Xiao-Fang Dong, Bin Cheng, Xiao-Jing Guo, Ting Du, Hong Wen, Xian-Zi Ji, Jia-Fu Cancer Manag Res Original Research BACKGROUND: Glucose-6-phosphate isomerase (GPI) is a glycolytic-related enzyme that inter-converts glucose-6-phosphate and fructose-6-phosphate in the cytoplasm. This protein is also secreted into the extracellular matrix by cancer cells and is, therefore, also called autocrine motility factor (AMF). METHODS: To clarify the roles of AMF/GPI in gastric cancer (GC), we collected 335 GC tissues and the corresponding adjacent noncancerous tissues, performed immunohistochemical studies, and analyzed the relationship between AMF/GPI expression and the patients’ clinicopathologic features. RESULTS: AMF/GPI expression was found to be significantly higher in the GC group than in the corresponding noncancerous tissue group (P<0.001). Additionally, AMF/GPI expression positively associated with a higher TNM stage and poorer prognosis in patients. Through Kaplan–Meier analysis and according to the Oncomine database, we found that AMF/GPI was overexpressed in GC tissues compared to normal mucosa, and the patients with higher AMF/GPI expression had poorer outcomes. We used AMF/GPI-silenced GC cell lines to observe how changes in AMP/GPI affect cellular phenotypes. AMF/GPI knockdown suppressed proliferation, migration, invasion, and glycolysis, and induced apoptosis in GC cells. CONCLUSION: These findings suggest that AMF/GPI overexpression is involved in carcinogenesis and promotes the aggressive phenotypes of GC cells. Dove Medical Press 2018-10-25 /pmc/articles/PMC6208529/ /pubmed/30464597 http://dx.doi.org/10.2147/CMAR.S177441 Text en © 2018 Ma et al. 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.
spellingShingle Original Research
Ma, Yu-Teng
Xing, Xiao-Fang
Dong, Bin
Cheng, Xiao-Jing
Guo, Ting
Du, Hong
Wen, Xian-Zi
Ji, Jia-Fu
Higher autocrine motility factor/glucose-6-phosphate isomerase expression is associated with tumorigenesis and poorer prognosis in gastric cancer
title Higher autocrine motility factor/glucose-6-phosphate isomerase expression is associated with tumorigenesis and poorer prognosis in gastric cancer
title_full Higher autocrine motility factor/glucose-6-phosphate isomerase expression is associated with tumorigenesis and poorer prognosis in gastric cancer
title_fullStr Higher autocrine motility factor/glucose-6-phosphate isomerase expression is associated with tumorigenesis and poorer prognosis in gastric cancer
title_full_unstemmed Higher autocrine motility factor/glucose-6-phosphate isomerase expression is associated with tumorigenesis and poorer prognosis in gastric cancer
title_short Higher autocrine motility factor/glucose-6-phosphate isomerase expression is associated with tumorigenesis and poorer prognosis in gastric cancer
title_sort higher autocrine motility factor/glucose-6-phosphate isomerase expression is associated with tumorigenesis and poorer prognosis in gastric cancer
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6208529/
https://www.ncbi.nlm.nih.gov/pubmed/30464597
http://dx.doi.org/10.2147/CMAR.S177441
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