The Proline Regulatory Axis and Cancer
Studies in metabolism and cancer have characterized changes in core pathways involving glucose and glutamine, emphasizing the provision of substrates for building cell mass. But recent findings suggest that pathways previously considered peripheral may play a critical role providing mechanisms for c...
Main Authors: | , , , |
---|---|
Format: | Online |
Language: | English |
Published: |
Frontiers Research Foundation
2012
|
Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3380417/ |
id |
pubmed-3380417 |
---|---|
recordtype |
oai_dc |
spelling |
pubmed-33804172012-06-25 The Proline Regulatory Axis and Cancer Phang, James Ming Liu, Wei Hancock, Chad Christian, Kyle J. Oncology Studies in metabolism and cancer have characterized changes in core pathways involving glucose and glutamine, emphasizing the provision of substrates for building cell mass. But recent findings suggest that pathways previously considered peripheral may play a critical role providing mechanisms for cell regulation. Several of these mechanisms involve the metabolism of non-essential amino acids, for example, the channeling of glycolytic intermediates into the serine pathway for one-carbon transfers. Historically, we proposed that the proline biosynthetic pathway participated in a metabolic interlock with glucose metabolism. The discovery that proline degradation is activated by p53 directed our attention to the initiation of apoptosis by proline oxidase/dehydrogenase. Now, however, we find that the biosynthetic mechanisms and the metabolic interlock may depend on the pathway from glutamine to proline, and it is markedly activated by the oncogene MYC. These findings add a new dimension to the proline regulatory axis in cancer and present attractive potential targets for cancer treatment. Frontiers Research Foundation 2012-06-21 /pmc/articles/PMC3380417/ /pubmed/22737668 http://dx.doi.org/10.3389/fonc.2012.00060 Text en Copyright © 2012 Phang, Liu, Hancock and Christian. http://www.frontiersin.org/licenseagreement This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited. |
repository_type |
Open Access Journal |
institution_category |
Foreign Institution |
institution |
US National Center for Biotechnology Information |
building |
NCBI PubMed |
collection |
Online Access |
language |
English |
format |
Online |
author |
Phang, James Ming Liu, Wei Hancock, Chad Christian, Kyle J. |
spellingShingle |
Phang, James Ming Liu, Wei Hancock, Chad Christian, Kyle J. The Proline Regulatory Axis and Cancer |
author_facet |
Phang, James Ming Liu, Wei Hancock, Chad Christian, Kyle J. |
author_sort |
Phang, James Ming |
title |
The Proline Regulatory Axis and Cancer |
title_short |
The Proline Regulatory Axis and Cancer |
title_full |
The Proline Regulatory Axis and Cancer |
title_fullStr |
The Proline Regulatory Axis and Cancer |
title_full_unstemmed |
The Proline Regulatory Axis and Cancer |
title_sort |
proline regulatory axis and cancer |
description |
Studies in metabolism and cancer have characterized changes in core pathways involving glucose and glutamine, emphasizing the provision of substrates for building cell mass. But recent findings suggest that pathways previously considered peripheral may play a critical role providing mechanisms for cell regulation. Several of these mechanisms involve the metabolism of non-essential amino acids, for example, the channeling of glycolytic intermediates into the serine pathway for one-carbon transfers. Historically, we proposed that the proline biosynthetic pathway participated in a metabolic interlock with glucose metabolism. The discovery that proline degradation is activated by p53 directed our attention to the initiation of apoptosis by proline oxidase/dehydrogenase. Now, however, we find that the biosynthetic mechanisms and the metabolic interlock may depend on the pathway from glutamine to proline, and it is markedly activated by the oncogene MYC. These findings add a new dimension to the proline regulatory axis in cancer and present attractive potential targets for cancer treatment. |
publisher |
Frontiers Research Foundation |
publishDate |
2012 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3380417/ |
_version_ |
1611538390194323456 |