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Metabolic Plasticity in Cancer Cells: Reconnecting Mitochondrial Function to Cancer Control
Anomalous increase in glycolytic activity defines one of the key metabolic alterations in cancer cells. A realization of this feature has led to critical advancements in cancer detection techniques such as positron emission tomography (PET) as well as a number of therapeutic avenues targeting the ke...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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2015
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4598183/ https://www.ncbi.nlm.nih.gov/pubmed/26457230 http://dx.doi.org/10.4172/2157-7013.1000211 |
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author | Ramanujan, V. Krishnan |
author_facet | Ramanujan, V. Krishnan |
author_sort | Ramanujan, V. Krishnan |
collection | PubMed |
description | Anomalous increase in glycolytic activity defines one of the key metabolic alterations in cancer cells. A realization of this feature has led to critical advancements in cancer detection techniques such as positron emission tomography (PET) as well as a number of therapeutic avenues targeting the key glycolytic steps within a cancer cell. A normal healthy cell’s survival relies on a sensitive balance between the primordial glycolysis and a more regulated mitochondrial bioenergetics. The salient difference between these two bioenergetics pathways is that oxygen availability is an obligatory requirement for mitochondrial pathway while glycolysis can function without oxygen. Early observations that some cancer cells up-regulate glycolytic activity even in the presence of oxygen (aerobic glycolysis) led to a hypothesis that such an altered cancer cell metabolism stems from inherent mitochondrial dysfunction. While a general validity of this hypothesis is still being debated, a number of recent research efforts have yielded clarity on the physiological origins of this aerobic glycolysis phenotype in cancer cells. Building on these recent studies, we present a generalized scheme of cancer cell metabolism and propose a novel hypothesis that might rationalize new avenues of cancer intervention. |
format | Online Article Text |
id | pubmed-4598183 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
record_format | MEDLINE/PubMed |
spelling | pubmed-45981832015-10-08 Metabolic Plasticity in Cancer Cells: Reconnecting Mitochondrial Function to Cancer Control Ramanujan, V. Krishnan J Cell Sci Ther Article Anomalous increase in glycolytic activity defines one of the key metabolic alterations in cancer cells. A realization of this feature has led to critical advancements in cancer detection techniques such as positron emission tomography (PET) as well as a number of therapeutic avenues targeting the key glycolytic steps within a cancer cell. A normal healthy cell’s survival relies on a sensitive balance between the primordial glycolysis and a more regulated mitochondrial bioenergetics. The salient difference between these two bioenergetics pathways is that oxygen availability is an obligatory requirement for mitochondrial pathway while glycolysis can function without oxygen. Early observations that some cancer cells up-regulate glycolytic activity even in the presence of oxygen (aerobic glycolysis) led to a hypothesis that such an altered cancer cell metabolism stems from inherent mitochondrial dysfunction. While a general validity of this hypothesis is still being debated, a number of recent research efforts have yielded clarity on the physiological origins of this aerobic glycolysis phenotype in cancer cells. Building on these recent studies, we present a generalized scheme of cancer cell metabolism and propose a novel hypothesis that might rationalize new avenues of cancer intervention. 2015-06-22 2015-06 /pmc/articles/PMC4598183/ /pubmed/26457230 http://dx.doi.org/10.4172/2157-7013.1000211 Text en http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Article Ramanujan, V. Krishnan Metabolic Plasticity in Cancer Cells: Reconnecting Mitochondrial Function to Cancer Control |
title | Metabolic Plasticity in Cancer Cells: Reconnecting Mitochondrial Function to Cancer Control |
title_full | Metabolic Plasticity in Cancer Cells: Reconnecting Mitochondrial Function to Cancer Control |
title_fullStr | Metabolic Plasticity in Cancer Cells: Reconnecting Mitochondrial Function to Cancer Control |
title_full_unstemmed | Metabolic Plasticity in Cancer Cells: Reconnecting Mitochondrial Function to Cancer Control |
title_short | Metabolic Plasticity in Cancer Cells: Reconnecting Mitochondrial Function to Cancer Control |
title_sort | metabolic plasticity in cancer cells: reconnecting mitochondrial function to cancer control |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4598183/ https://www.ncbi.nlm.nih.gov/pubmed/26457230 http://dx.doi.org/10.4172/2157-7013.1000211 |
work_keys_str_mv | AT ramanujanvkrishnan metabolicplasticityincancercellsreconnectingmitochondrialfunctiontocancercontrol |