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Metabolic Reprogramming in Cancer Is Induced to Increase Proton Production

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Bibliographische Detailangaben
Zeitschriftentitel: Cancer Research
Personen und Körperschaften: Sun, Huiyan, Zhou, Yi, Skaro, Michael Francis, Wu, Yiran, Qu, Zexing, Mao, Fenglou, Zhao, Suwen, Xu, Ying
In: Cancer Research, 80, 2020, 5, S. 1143-1155
Format: E-Article
Sprache: Englisch
veröffentlicht:
American Association for Cancer Research (AACR)
Schlagwörter:
Cancer Research
Oncology
author_facet Sun, Huiyan
Zhou, Yi
Skaro, Michael Francis
Wu, Yiran
Qu, Zexing
Mao, Fenglou
Zhao, Suwen
Xu, Ying
Sun, Huiyan
Zhou, Yi
Skaro, Michael Francis
Wu, Yiran
Qu, Zexing
Mao, Fenglou
Zhao, Suwen
Xu, Ying
author Sun, Huiyan
Zhou, Yi
Skaro, Michael Francis
Wu, Yiran
Qu, Zexing
Mao, Fenglou
Zhao, Suwen
Xu, Ying
spellingShingle Sun, Huiyan
Zhou, Yi
Skaro, Michael Francis
Wu, Yiran
Qu, Zexing
Mao, Fenglou
Zhao, Suwen
Xu, Ying
Cancer Research
Metabolic Reprogramming in Cancer Is Induced to Increase Proton Production
Cancer Research
Oncology
author_sort sun, huiyan
spelling Sun, Huiyan Zhou, Yi Skaro, Michael Francis Wu, Yiran Qu, Zexing Mao, Fenglou Zhao, Suwen Xu, Ying 0008-5472 1538-7445 American Association for Cancer Research (AACR) Cancer Research Oncology http://dx.doi.org/10.1158/0008-5472.can-19-3392 <jats:title>Abstract</jats:title> <jats:sec> <jats:title /> <jats:p>Considerable metabolic reprogramming has been observed in a conserved manner across multiple cancer types, but their true causes remain elusive. We present an analysis of around 50 such reprogrammed metabolisms (RM) including the Warburg effect, nucleotide de novo synthesis, and sialic acid biosynthesis in cancer. Analyses of the biochemical reactions conducted by these RMs, coupled with gene expression data of their catalyzing enzymes, in 7,011 tissues of 14 cancer types, revealed that all RMs produce more H+ than their original metabolisms. These data strongly support a model that these RMs are induced or selected to neutralize a persistent intracellular alkaline stress due to chronic inflammation and local iron overload. To sustain these RMs for survival, cells must find metabolic exits for the nonproton products of these RMs in a continuous manner, some of which pose major challenges, such as nucleotides and sialic acids, because they are electrically charged. This analysis strongly suggests that continuous cell division and other cancerous behaviors are ways for the affected cells to remove such products in a timely and sustained manner. As supporting evidence, this model can offer simple and natural explanations to a range of long-standing open questions in cancer research including the cause of the Warburg effect.</jats:p> </jats:sec> <jats:sec> <jats:title>Significance:</jats:title> <jats:p>Inhibiting acidifying metabolic reprogramming could be a novel strategy for treating cancer.</jats:p> </jats:sec> Metabolic Reprogramming in Cancer Is Induced to Increase Proton Production Cancer Research
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title Metabolic Reprogramming in Cancer Is Induced to Increase Proton Production
title_unstemmed Metabolic Reprogramming in Cancer Is Induced to Increase Proton Production
title_full Metabolic Reprogramming in Cancer Is Induced to Increase Proton Production
title_fullStr Metabolic Reprogramming in Cancer Is Induced to Increase Proton Production
title_full_unstemmed Metabolic Reprogramming in Cancer Is Induced to Increase Proton Production
title_short Metabolic Reprogramming in Cancer Is Induced to Increase Proton Production
title_sort metabolic reprogramming in cancer is induced to increase proton production
topic Cancer Research
Oncology
url http://dx.doi.org/10.1158/0008-5472.can-19-3392
publishDate 2020
physical 1143-1155
description <jats:title>Abstract</jats:title> <jats:sec> <jats:title /> <jats:p>Considerable metabolic reprogramming has been observed in a conserved manner across multiple cancer types, but their true causes remain elusive. We present an analysis of around 50 such reprogrammed metabolisms (RM) including the Warburg effect, nucleotide de novo synthesis, and sialic acid biosynthesis in cancer. Analyses of the biochemical reactions conducted by these RMs, coupled with gene expression data of their catalyzing enzymes, in 7,011 tissues of 14 cancer types, revealed that all RMs produce more H+ than their original metabolisms. These data strongly support a model that these RMs are induced or selected to neutralize a persistent intracellular alkaline stress due to chronic inflammation and local iron overload. To sustain these RMs for survival, cells must find metabolic exits for the nonproton products of these RMs in a continuous manner, some of which pose major challenges, such as nucleotides and sialic acids, because they are electrically charged. This analysis strongly suggests that continuous cell division and other cancerous behaviors are ways for the affected cells to remove such products in a timely and sustained manner. As supporting evidence, this model can offer simple and natural explanations to a range of long-standing open questions in cancer research including the cause of the Warburg effect.</jats:p> </jats:sec> <jats:sec> <jats:title>Significance:</jats:title> <jats:p>Inhibiting acidifying metabolic reprogramming could be a novel strategy for treating cancer.</jats:p> </jats:sec>
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author Sun, Huiyan, Zhou, Yi, Skaro, Michael Francis, Wu, Yiran, Qu, Zexing, Mao, Fenglou, Zhao, Suwen, Xu, Ying
author_facet Sun, Huiyan, Zhou, Yi, Skaro, Michael Francis, Wu, Yiran, Qu, Zexing, Mao, Fenglou, Zhao, Suwen, Xu, Ying, Sun, Huiyan, Zhou, Yi, Skaro, Michael Francis, Wu, Yiran, Qu, Zexing, Mao, Fenglou, Zhao, Suwen, Xu, Ying
author_sort sun, huiyan
container_issue 5
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description <jats:title>Abstract</jats:title> <jats:sec> <jats:title /> <jats:p>Considerable metabolic reprogramming has been observed in a conserved manner across multiple cancer types, but their true causes remain elusive. We present an analysis of around 50 such reprogrammed metabolisms (RM) including the Warburg effect, nucleotide de novo synthesis, and sialic acid biosynthesis in cancer. Analyses of the biochemical reactions conducted by these RMs, coupled with gene expression data of their catalyzing enzymes, in 7,011 tissues of 14 cancer types, revealed that all RMs produce more H+ than their original metabolisms. These data strongly support a model that these RMs are induced or selected to neutralize a persistent intracellular alkaline stress due to chronic inflammation and local iron overload. To sustain these RMs for survival, cells must find metabolic exits for the nonproton products of these RMs in a continuous manner, some of which pose major challenges, such as nucleotides and sialic acids, because they are electrically charged. This analysis strongly suggests that continuous cell division and other cancerous behaviors are ways for the affected cells to remove such products in a timely and sustained manner. As supporting evidence, this model can offer simple and natural explanations to a range of long-standing open questions in cancer research including the cause of the Warburg effect.</jats:p> </jats:sec> <jats:sec> <jats:title>Significance:</jats:title> <jats:p>Inhibiting acidifying metabolic reprogramming could be a novel strategy for treating cancer.</jats:p> </jats:sec>
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spelling Sun, Huiyan Zhou, Yi Skaro, Michael Francis Wu, Yiran Qu, Zexing Mao, Fenglou Zhao, Suwen Xu, Ying 0008-5472 1538-7445 American Association for Cancer Research (AACR) Cancer Research Oncology http://dx.doi.org/10.1158/0008-5472.can-19-3392 <jats:title>Abstract</jats:title> <jats:sec> <jats:title /> <jats:p>Considerable metabolic reprogramming has been observed in a conserved manner across multiple cancer types, but their true causes remain elusive. We present an analysis of around 50 such reprogrammed metabolisms (RM) including the Warburg effect, nucleotide de novo synthesis, and sialic acid biosynthesis in cancer. Analyses of the biochemical reactions conducted by these RMs, coupled with gene expression data of their catalyzing enzymes, in 7,011 tissues of 14 cancer types, revealed that all RMs produce more H+ than their original metabolisms. These data strongly support a model that these RMs are induced or selected to neutralize a persistent intracellular alkaline stress due to chronic inflammation and local iron overload. To sustain these RMs for survival, cells must find metabolic exits for the nonproton products of these RMs in a continuous manner, some of which pose major challenges, such as nucleotides and sialic acids, because they are electrically charged. This analysis strongly suggests that continuous cell division and other cancerous behaviors are ways for the affected cells to remove such products in a timely and sustained manner. As supporting evidence, this model can offer simple and natural explanations to a range of long-standing open questions in cancer research including the cause of the Warburg effect.</jats:p> </jats:sec> <jats:sec> <jats:title>Significance:</jats:title> <jats:p>Inhibiting acidifying metabolic reprogramming could be a novel strategy for treating cancer.</jats:p> </jats:sec> Metabolic Reprogramming in Cancer Is Induced to Increase Proton Production Cancer Research
spellingShingle Sun, Huiyan, Zhou, Yi, Skaro, Michael Francis, Wu, Yiran, Qu, Zexing, Mao, Fenglou, Zhao, Suwen, Xu, Ying, Cancer Research, Metabolic Reprogramming in Cancer Is Induced to Increase Proton Production, Cancer Research, Oncology
title Metabolic Reprogramming in Cancer Is Induced to Increase Proton Production
title_full Metabolic Reprogramming in Cancer Is Induced to Increase Proton Production
title_fullStr Metabolic Reprogramming in Cancer Is Induced to Increase Proton Production
title_full_unstemmed Metabolic Reprogramming in Cancer Is Induced to Increase Proton Production
title_short Metabolic Reprogramming in Cancer Is Induced to Increase Proton Production
title_sort metabolic reprogramming in cancer is induced to increase proton production
title_unstemmed Metabolic Reprogramming in Cancer Is Induced to Increase Proton Production
topic Cancer Research, Oncology
url http://dx.doi.org/10.1158/0008-5472.can-19-3392