Glycolytic suppression dramatically changes the intracellular metabolic profile of multiple cancer cell lines in a mitochondrial metabolism-dependent manner
Identifieur interne : 000792 ( Main/Exploration ); précédent : 000791; suivant : 000793Glycolytic suppression dramatically changes the intracellular metabolic profile of multiple cancer cell lines in a mitochondrial metabolism-dependent manner
Auteurs : Reika Shiratori ; Kenta Furuichi ; Masashi Yamaguchi ; Natsumi Miyazaki ; Haruna Aoki ; Hiroji Chibana ; Kousei Ito ; Shigeki AokiSource :
- Scientific Reports [ 2045-2322 ] ; 2019.
Abstract
Most cancer cells rely on glycolysis to generate ATP, even when oxygen is available. However, merely inhibiting the glycolysis is insufficient for the eradication of cancer cells. One main reason for this is that cancer cells have the potential to adapt their metabolism to their environmental conditions. In this study, we investigated how cancer cells modify their intracellular metabolism when glycolysis is suppressed, using PANC-1 pancreatic cancer cells and two other solid tumor cell lines, A549 and HeLa. Our study revealed that glycolytically suppressed cells upregulated mitochondrial function and relied on oxidative phosphorylation (OXPHOS) to obtain the ATP necessary for their survival. Dynamic changes in intracellular metabolic profiles were also observed, reflected by the reduced levels of TCA cycle intermediates and elevated levels of most amino acids. Glutamine and glutamate were important for this metabolic reprogramming, as these were largely consumed by influx into the TCA cycle when the glycolytic pathway was suppressed. During the reprogramming process, activated autophagy was involved in modulating mitochondrial function. We conclude that upon glycolytic suppression in multiple types of tumor cells, intracellular energy metabolism is reprogrammed toward mitochondrial OXPHOS in an autophagy-dependent manner to ensure cellular survival.
Url:
DOI: 10.1038/s41598-019-55296-3
PubMed: 31822748
PubMed Central: 6904735
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en"><p id="Par1">Most cancer cells rely on glycolysis to generate ATP, even when oxygen is available. However, merely inhibiting the glycolysis is insufficient for the eradication of cancer cells. One main reason for this is that cancer cells have the potential to adapt their metabolism to their environmental conditions. In this study, we investigated how cancer cells modify their intracellular metabolism when glycolysis is suppressed, using PANC-1 pancreatic cancer cells and two other solid tumor cell lines, A549 and HeLa. Our study revealed that glycolytically suppressed cells upregulated mitochondrial function and relied on oxidative phosphorylation (OXPHOS) to obtain the ATP necessary for their survival. Dynamic changes in intracellular metabolic profiles were also observed, reflected by the reduced levels of TCA cycle intermediates and elevated levels of most amino acids. Glutamine and glutamate were important for this metabolic reprogramming, as these were largely consumed by influx into the TCA cycle when the glycolytic pathway was suppressed. During the reprogramming process, activated autophagy was involved in modulating mitochondrial function. We conclude that upon glycolytic suppression in multiple types of tumor cells, intracellular energy metabolism is reprogrammed toward mitochondrial OXPHOS in an autophagy-dependent manner to ensure cellular survival.</p>
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<tree><noCountry><name sortKey="Aoki, Haruna" sort="Aoki, Haruna" uniqKey="Aoki H" first="Haruna" last="Aoki">Haruna Aoki</name>
<name sortKey="Aoki, Shigeki" sort="Aoki, Shigeki" uniqKey="Aoki S" first="Shigeki" last="Aoki">Shigeki Aoki</name>
<name sortKey="Chibana, Hiroji" sort="Chibana, Hiroji" uniqKey="Chibana H" first="Hiroji" last="Chibana">Hiroji Chibana</name>
<name sortKey="Furuichi, Kenta" sort="Furuichi, Kenta" uniqKey="Furuichi K" first="Kenta" last="Furuichi">Kenta Furuichi</name>
<name sortKey="Ito, Kousei" sort="Ito, Kousei" uniqKey="Ito K" first="Kousei" last="Ito">Kousei Ito</name>
<name sortKey="Miyazaki, Natsumi" sort="Miyazaki, Natsumi" uniqKey="Miyazaki N" first="Natsumi" last="Miyazaki">Natsumi Miyazaki</name>
<name sortKey="Shiratori, Reika" sort="Shiratori, Reika" uniqKey="Shiratori R" first="Reika" last="Shiratori">Reika Shiratori</name>
<name sortKey="Yamaguchi, Masashi" sort="Yamaguchi, Masashi" uniqKey="Yamaguchi M" first="Masashi" last="Yamaguchi">Masashi Yamaguchi</name>
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