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Tumor pyruvate kinase M2: A promising molecular target of gastrointestinal cancer

Gastrointestinal (GI) cancer is one of the most common causes of cancer-related deaths worldwide. Tumor markers are valuable in detecting post-surgical recurrence or in monitoring response to chemotherapy. Pyruvate kinase isoform M2 (PKM2), a glycolytic enzyme catalyzing conversion of phosphoenolpyr...

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Detalles Bibliográficos
Autores principales: Guo, Chen, Li, Guan, Hou, Jianing, Deng, Xingming, Ao, Sheng, Li, Zhuofei, Lyu, Guoqing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AME Publishing Company 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6328500/
https://www.ncbi.nlm.nih.gov/pubmed/30700935
http://dx.doi.org/10.21147/j.issn.1000-9604.2018.06.11
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author Guo, Chen
Li, Guan
Hou, Jianing
Deng, Xingming
Ao, Sheng
Li, Zhuofei
Lyu, Guoqing
author_facet Guo, Chen
Li, Guan
Hou, Jianing
Deng, Xingming
Ao, Sheng
Li, Zhuofei
Lyu, Guoqing
author_sort Guo, Chen
collection PubMed
description Gastrointestinal (GI) cancer is one of the most common causes of cancer-related deaths worldwide. Tumor markers are valuable in detecting post-surgical recurrence or in monitoring response to chemotherapy. Pyruvate kinase isoform M2 (PKM2), a glycolytic enzyme catalyzing conversion of phosphoenolpyruvate (PEP) to pyruvate, confers a growth advantage to the tumor cells and enables them to adapt to the tumor microenvironment. In this review, we have summarized current research on the expression and regulation of PKM2 in tumor cells, and its potential role in GI carcinogenesis and progression. Furthermore, we have also discussed the potential of PKM2 as a diagnostic and screening marker, and a therapeutic target in GI cancer.
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spelling pubmed-63285002019-01-30 Tumor pyruvate kinase M2: A promising molecular target of gastrointestinal cancer Guo, Chen Li, Guan Hou, Jianing Deng, Xingming Ao, Sheng Li, Zhuofei Lyu, Guoqing Chin J Cancer Res Review Article Gastrointestinal (GI) cancer is one of the most common causes of cancer-related deaths worldwide. Tumor markers are valuable in detecting post-surgical recurrence or in monitoring response to chemotherapy. Pyruvate kinase isoform M2 (PKM2), a glycolytic enzyme catalyzing conversion of phosphoenolpyruvate (PEP) to pyruvate, confers a growth advantage to the tumor cells and enables them to adapt to the tumor microenvironment. In this review, we have summarized current research on the expression and regulation of PKM2 in tumor cells, and its potential role in GI carcinogenesis and progression. Furthermore, we have also discussed the potential of PKM2 as a diagnostic and screening marker, and a therapeutic target in GI cancer. AME Publishing Company 2018-12 /pmc/articles/PMC6328500/ /pubmed/30700935 http://dx.doi.org/10.21147/j.issn.1000-9604.2018.06.11 Text en Copyright © 2018 Chinese Journal of Cancer Research. All rights reserved. http://creativecommons.org/licenses/by-nc-sa/4.0/ This work is licensed under a Creative Commons Attribution-Non Commercial-Share Alike 4.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/4.0/
spellingShingle Review Article
Guo, Chen
Li, Guan
Hou, Jianing
Deng, Xingming
Ao, Sheng
Li, Zhuofei
Lyu, Guoqing
Tumor pyruvate kinase M2: A promising molecular target of gastrointestinal cancer
title Tumor pyruvate kinase M2: A promising molecular target of gastrointestinal cancer
title_full Tumor pyruvate kinase M2: A promising molecular target of gastrointestinal cancer
title_fullStr Tumor pyruvate kinase M2: A promising molecular target of gastrointestinal cancer
title_full_unstemmed Tumor pyruvate kinase M2: A promising molecular target of gastrointestinal cancer
title_short Tumor pyruvate kinase M2: A promising molecular target of gastrointestinal cancer
title_sort tumor pyruvate kinase m2: a promising molecular target of gastrointestinal cancer
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6328500/
https://www.ncbi.nlm.nih.gov/pubmed/30700935
http://dx.doi.org/10.21147/j.issn.1000-9604.2018.06.11
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