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000125881 1001_ $$0P:(DE-He78)0e1771fdf6e4f108d2d435315ecd900e$$aGdynia, Georg Przemyslaw$$b0$$eFirst author$$udkfz
000125881 245__ $$aThe HMGB1 protein induces a metabolic type of tumour cell death by blocking aerobic respiration.
000125881 260__ $$aLondon$$bNature Publishing Group$$c2016
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000125881 520__ $$aThe high-mobility group box 1 (HMGB1) protein has a central role in immunological antitumour defense. Here we show that natural killer cell-derived HMGB1 directly eliminates cancer cells by triggering metabolic cell death. HMGB1 allosterically inhibits the tetrameric pyruvate kinase isoform M2, thus blocking glucose-driven aerobic respiration. This results in a rapid metabolic shift forcing cells to rely solely on glycolysis for the maintenance of energy production. Cancer cells can acquire resistance to HMGB1 by increasing glycolysis using the dimeric form of PKM2, and employing glutaminolysis. Consistently, we observe an increase in the expression of a key enzyme of glutaminolysis, malic enzyme 1, in advanced colon cancer. Moreover, pharmaceutical inhibition of glutaminolysis sensitizes tumour cells to HMGB1 providing a basis for a therapeutic strategy for treating cancer.
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000125881 650_7 $$2NLM Chemicals$$aCarrier Proteins
000125881 650_7 $$2NLM Chemicals$$aHMGB1 Protein
000125881 650_7 $$2NLM Chemicals$$aMembrane Proteins
000125881 650_7 $$2NLM Chemicals$$aThyroid Hormones
000125881 650_7 $$2NLM Chemicals$$athyroid hormone-binding proteins
000125881 650_7 $$0IY9XDZ35W2$$2NLM Chemicals$$aGlucose
000125881 7001_ $$aSauer, Sven W$$b1
000125881 7001_ $$0P:(DE-HGF)0$$aKopitz, Jürgen$$b2
000125881 7001_ $$aFuchs, Dominik$$b3
000125881 7001_ $$aDuglova, Katarina$$b4
000125881 7001_ $$aRuppert, Thorsten$$b5
000125881 7001_ $$0P:(DE-HGF)0$$aMiller, Matthias$$b6
000125881 7001_ $$0P:(DE-He78)0f643e43f006f9ce6666909ec4f79a2f$$aPahl, Jens$$b7$$udkfz
000125881 7001_ $$0P:(DE-He78)d2b4dd8bdffe4aaa0f5e30e91587766f$$aCerwenka, Adelheid$$b8$$udkfz
000125881 7001_ $$aEnders, Markus$$b9
000125881 7001_ $$aMairbäurl, Heimo$$b10
000125881 7001_ $$0P:(DE-HGF)0$$aKamiński, Marcin M$$b11
000125881 7001_ $$aPenzel, Roland$$b12
000125881 7001_ $$aZhang, Christine$$b13
000125881 7001_ $$aFuller, Jonathan C$$b14
000125881 7001_ $$aWade, Rebecca C$$b15
000125881 7001_ $$0P:(DE-He78)e15dfa1260625c69d6690a197392a994$$aBenner, Axel$$b16$$udkfz
000125881 7001_ $$0P:(DE-He78)c259d6cc99edf5c7bc7ce22c7f87c253$$aChang, Jenny$$b17$$udkfz
000125881 7001_ $$0P:(DE-He78)90d5535ff896e70eed81f4a4f6f22ae2$$aBrenner, Hermann$$b18$$udkfz
000125881 7001_ $$0P:(DE-He78)6c5d058b7552d071a7fa4c5e943fff0f$$aHoffmeister, Michael$$b19$$udkfz
000125881 7001_ $$0P:(DE-HGF)0$$aZentgraf, Hanswalter$$b20
000125881 7001_ $$aSchirmacher, Peter$$b21
000125881 7001_ $$0P:(DE-He78)6c54d919bb3371b6d7f277e2c6262a4a$$aRoth, Wilfried$$b22$$eLast author$$udkfz
000125881 773__ $$0PERI:(DE-600)2553671-0$$a10.1038/ncomms10764$$gVol. 7, p. 10764 -$$p10764 -$$tNature Communications$$v7$$x2041-1723$$y2016
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