The metabolic function of cyclin D3–CDK6 kinase in cancer cell survival
The cyclin D3–CDK6 kinase complex, which is overactive in some cancers, inhibits two key glycolysis enzymes and thereby enhances the levels of antioxidants in cells, promoting tumour cell survival. Cancer cell survival by cyclin D3–CDK6 metabolism Cyclin–CDK complexes are commonly amplified in cance...
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| Vydáno v: | Nature (London) Ročník 546; číslo 7658; s. 426 - 430 |
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| Hlavní autoři: | , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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London
Nature Publishing Group UK
15.06.2017
Nature Publishing Group |
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| ISSN: | 0028-0836, 1476-4687, 1476-4687 |
| On-line přístup: | Získat plný text |
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| Abstract | The cyclin D3–CDK6 kinase complex, which is overactive in some cancers, inhibits two key glycolysis enzymes and thereby enhances the levels of antioxidants in cells, promoting tumour cell survival.
Cancer cell survival by cyclin D3–CDK6 metabolism
Cyclin–CDK complexes are commonly amplified in cancer and promote cell cycle progression. Inhibitors for CDK4/6 are being tested in clinical trials and are thought to work in patients that retain expression of the CDK substrate RB1. Here, the authors describe an additional pro-survival role of one cyclin–CDK complex, D3–CDK6, which controls cellular metabolism. When hyperactivated in cancer cells, the complex phosphorylates and inactivates two glycolysis enzymes. This redirects glycolytic intermediates to the pentose phosphate and serine pathways, providing enhanced antioxidant capacity. CDK4/6 inhibitors can induce apoptosis by increasing the oxidative stress in tumour cells expressing high levels of D3–CDK6 complexes. The findings suggest that, in addition to RB1, markers such as levels of D3–CDK6 complexes could be useful for identifying patients likely to respond to CDK4/6 inhibitors.
D-type cyclins (D1, D2 and D3) and their associated cyclin-dependent kinases (CDK4 and CDK6) are components of the core cell cycle machinery that drives cell proliferation
1
,
2
. Inhibitors of CDK4 and CDK6 are currently being tested in clinical trials for patients with several cancer types, with promising results
2
. Here, using human cancer cells and patient-derived xenografts in mice, we show that the cyclin D3–CDK6 kinase phosphorylates and inhibits the catalytic activity of two key enzymes in the glycolytic pathway, 6-phosphofructokinase and pyruvate kinase M2. This re-directs the glycolytic intermediates into the pentose phosphate (PPP) and serine pathways. Inhibition of cyclin D3–CDK6 in tumour cells reduces flow through the PPP and serine pathways, thereby depleting the antioxidants NADPH and glutathione. This, in turn, increases the levels of reactive oxygen species and causes apoptosis of tumour cells. The pro-survival function of cyclin D-associated kinase operates in tumours expressing high levels of cyclin D3–CDK6 complexes. We propose that measuring the levels of cyclin D3–CDK6 in human cancers might help to identify tumour subsets that undergo cell death and tumour regression upon inhibition of CDK4 and CDK6. Cyclin D3–CDK6, through its ability to link cell cycle and cell metabolism, represents a particularly powerful oncoprotein that affects cancer cells at several levels, and this property can be exploited for anti-cancer therapy. |
|---|---|
| AbstractList | D-type cyclins (D1, D2 and D3) and their associated cyclindependent kinases (CDK4 and CDK6) are components of the core cell cycle machinery that drives cell proliferation1,2. Inhibitors of CDK4 and CDK6 are currently being tested in clinical trials for patients with several cancer types, with promising results2. Here, using human cancer cells and patient-derived xenografts in mice, we show that the cyclin D3-CDK6 kinase phosphorylates and inhibits the catalytic activity of two key enzymes in the glycolytic pathway, 6-phosphofructokinase and pyruvate kinase M2. This re-directs the glycolytic intermediates into the pentose phosphate (PPP) and serine pathways. Inhibition of cyclin D3-CDK6 in tumour cells reduces flow through the PPP and serine pathways, thereby depleting the antioxidants NADPH and glutathione. This, in turn, increases the levels of reactive oxygen species and causes apoptosis of tumour cells. The pro-survival function of cyclin D-associated kinase operates in tumours expressing high levels of cyclin D3-CDK6 complexes. We propose that measuring the levels of cyclin D3-CDK6 in human cancers might help to identify tumour subsets that undergo cell death and tumour regression upon inhibition of CDK4 and CDK6. Cyclin D3-CDK6, through its ability to link cell cycle and cell metabolism, represents a particularly powerful oncoprotein that affects cancer cells at several levels, and this property can be exploited for anti-cancer therapy. D-type cyclins (D1, D2 and D3) together with their associated cyclin-dependent kinases CDK4 and CDK6 are components of the core cell cycle machinery that drives cell proliferation1,2. Inhibitors of CDK4 and CDK6 are currently in clinical trials for patients with several cancer types, with promising results2. Here, we show that cyclin D3-CDK6 phosphorylates and inhibits the catalytic activity of two key enzymes in the glycolytic pathway, 6-phosphofructokinase and pyruvate kinase M2. This re-directs the glycolytic intermediates into the pentose phosphate (PPP) and serine pathways. Inhibition of cyclin D3-CDK6 in tumor cells reduces PPP and serine pathway flows, thereby depleting anti-oxidants NADPH and glutathione. This, in turn elevates the levels of reactive oxygen species and causes tumor cell apoptosis. The pro-survival function of cyclin D-associated kinase operates in tumors expressing high levels of cyclin D3-CDK6 complexes. We propose that measuring the levels of cyclin D3-CDK6 in human cancers might help to identify tumor subsets that undergo cell death and tumor regression upon CDK4/6-inhibition. Cyclin D3-CDK6, through its ability to link cell cycle and cell metabolism represents a particularly powerful oncogene that affects cancer cells at several levels, and this property can be exploited for anti-cancer therapy. D-type cyclins (D1, D2 and D3) and their associated cyclin-dependent kinases (CDK4 and CDK6) are components of the core cell cycle machinery that drives cell proliferation. Inhibitors of CDK4 and CDK6 are currently being tested in clinical trials for patients with several cancer types, with promising results. Here, using human cancer cells and patient-derived xenografts in mice, we show that the cyclin D3-CDK6 kinase phosphorylates and inhibits the catalytic activity of two key enzymes in the glycolytic pathway, 6-phosphofructokinase and pyruvate kinase M2. This re-directs the glycolytic intermediates into the pentose phosphate (PPP) and serine pathways. Inhibition of cyclin D3-CDK6 in tumour cells reduces flow through the PPP and serine pathways, thereby depleting the antioxidants NADPH and glutathione. This, in turn, increases the levels of reactive oxygen species and causes apoptosis of tumour cells. The pro-survival function of cyclin D-associated kinase operates in tumours expressing high levels of cyclin D3-CDK6 complexes. We propose that measuring the levels of cyclin D3-CDK6 in human cancers might help to identify tumour subsets that undergo cell death and tumour regression upon inhibition of CDK4 and CDK6. Cyclin D3-CDK6, through its ability to link cell cycle and cell metabolism, represents a particularly powerful oncoprotein that affects cancer cells at several levels, and this property can be exploited for anti-cancer therapy. The cyclin D3–CDK6 kinase complex, which is overactive in some cancers, inhibits two key glycolysis enzymes and thereby enhances the levels of antioxidants in cells, promoting tumour cell survival. Cancer cell survival by cyclin D3–CDK6 metabolism Cyclin–CDK complexes are commonly amplified in cancer and promote cell cycle progression. Inhibitors for CDK4/6 are being tested in clinical trials and are thought to work in patients that retain expression of the CDK substrate RB1. Here, the authors describe an additional pro-survival role of one cyclin–CDK complex, D3–CDK6, which controls cellular metabolism. When hyperactivated in cancer cells, the complex phosphorylates and inactivates two glycolysis enzymes. This redirects glycolytic intermediates to the pentose phosphate and serine pathways, providing enhanced antioxidant capacity. CDK4/6 inhibitors can induce apoptosis by increasing the oxidative stress in tumour cells expressing high levels of D3–CDK6 complexes. The findings suggest that, in addition to RB1, markers such as levels of D3–CDK6 complexes could be useful for identifying patients likely to respond to CDK4/6 inhibitors. D-type cyclins (D1, D2 and D3) and their associated cyclin-dependent kinases (CDK4 and CDK6) are components of the core cell cycle machinery that drives cell proliferation 1 , 2 . Inhibitors of CDK4 and CDK6 are currently being tested in clinical trials for patients with several cancer types, with promising results 2 . Here, using human cancer cells and patient-derived xenografts in mice, we show that the cyclin D3–CDK6 kinase phosphorylates and inhibits the catalytic activity of two key enzymes in the glycolytic pathway, 6-phosphofructokinase and pyruvate kinase M2. This re-directs the glycolytic intermediates into the pentose phosphate (PPP) and serine pathways. Inhibition of cyclin D3–CDK6 in tumour cells reduces flow through the PPP and serine pathways, thereby depleting the antioxidants NADPH and glutathione. This, in turn, increases the levels of reactive oxygen species and causes apoptosis of tumour cells. The pro-survival function of cyclin D-associated kinase operates in tumours expressing high levels of cyclin D3–CDK6 complexes. We propose that measuring the levels of cyclin D3–CDK6 in human cancers might help to identify tumour subsets that undergo cell death and tumour regression upon inhibition of CDK4 and CDK6. Cyclin D3–CDK6, through its ability to link cell cycle and cell metabolism, represents a particularly powerful oncoprotein that affects cancer cells at several levels, and this property can be exploited for anti-cancer therapy. D-type cyclins (D1, D2 and D3) and their associated cyclin-dependent kinases (CDK4 and CDK6) are components of the core cell cycle machinery that drives cell proliferation. Inhibitors of CDK4 and CDK6 are currently being tested in clinical trials for patients with several cancer types, with promising results. Here, using human cancer cells and patient-derived xenografts in mice, we show that the cyclin D3-CDK6 kinase phosphorylates and inhibits the catalytic activity of two key enzymes in the glycolytic pathway, 6-phosphofructokinase and pyruvate kinase M2. This re-directs the glycolytic intermediates into the pentose phosphate (PPP) and serine pathways. Inhibition of cyclin D3-CDK6 in tumour cells reduces flow through the PPP and serine pathways, thereby depleting the antioxidants NADPH and glutathione. This, in turn, increases the levels of reactive oxygen species and causes apoptosis of tumour cells. The pro-survival function of cyclin D-associated kinase operates in tumours expressing high levels of cyclin D3-CDK6 complexes. We propose that measuring the levels of cyclin D3-CDK6 in human cancers might help to identify tumour subsets that undergo cell death and tumour regression upon inhibition of CDK4 and CDK6. Cyclin D3-CDK6, through its ability to link cell cycle and cell metabolism, represents a particularly powerful oncoprotein that affects cancer cells at several levels, and this property can be exploited for anti-cancer therapy.D-type cyclins (D1, D2 and D3) and their associated cyclin-dependent kinases (CDK4 and CDK6) are components of the core cell cycle machinery that drives cell proliferation. Inhibitors of CDK4 and CDK6 are currently being tested in clinical trials for patients with several cancer types, with promising results. Here, using human cancer cells and patient-derived xenografts in mice, we show that the cyclin D3-CDK6 kinase phosphorylates and inhibits the catalytic activity of two key enzymes in the glycolytic pathway, 6-phosphofructokinase and pyruvate kinase M2. This re-directs the glycolytic intermediates into the pentose phosphate (PPP) and serine pathways. Inhibition of cyclin D3-CDK6 in tumour cells reduces flow through the PPP and serine pathways, thereby depleting the antioxidants NADPH and glutathione. This, in turn, increases the levels of reactive oxygen species and causes apoptosis of tumour cells. The pro-survival function of cyclin D-associated kinase operates in tumours expressing high levels of cyclin D3-CDK6 complexes. We propose that measuring the levels of cyclin D3-CDK6 in human cancers might help to identify tumour subsets that undergo cell death and tumour regression upon inhibition of CDK4 and CDK6. Cyclin D3-CDK6, through its ability to link cell cycle and cell metabolism, represents a particularly powerful oncoprotein that affects cancer cells at several levels, and this property can be exploited for anti-cancer therapy. |
| Author | Sicinski, Piotr Williams, Juliet A. Gao, Xueliang Geng, Yan Ren, Hong Gao, Hui Gerdemann, Ulrike Dyson, Nicholas J. Wang, Haizhen Gygi, Steven P. Chick, Joel M. Yang, Guizhi Polyak, Kornelia Keibler, Mark A. Sicinska, Ewa Haining, W. Nicholas Nicolay, Brandon N. Suski, Jan M. Roberts, Thomas M. |
| AuthorAffiliation | 3 Massachusetts General Hospital Cancer Center, Charlestown, Massachusetts 02129, USA 6 Novartis Institutes for Biomedical Research, Cambridge, Massachusetts 02139, USA 10 Division of Pediatric Hematology and Oncology, Children’s Hospital, Boston, Massachusetts 02115, USA 2 Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA 11 Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA 12 Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA 5 Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA 8 Department of Oncologic Pathology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA 7 Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139 USA 9 Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA 1 Department of Cancer Bi |
| AuthorAffiliation_xml | – name: 7 Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139 USA – name: 8 Department of Oncologic Pathology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA – name: 11 Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA – name: 10 Division of Pediatric Hematology and Oncology, Children’s Hospital, Boston, Massachusetts 02115, USA – name: 3 Massachusetts General Hospital Cancer Center, Charlestown, Massachusetts 02129, USA – name: 1 Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA – name: 12 Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA – name: 5 Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA – name: 9 Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA – name: 2 Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA – name: 6 Novartis Institutes for Biomedical Research, Cambridge, Massachusetts 02139, USA – name: 4 Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA |
| Author_xml | – sequence: 1 givenname: Haizhen surname: Wang fullname: Wang, Haizhen organization: Department of Cancer Biology, Dana-Farber Cancer Institute, Department of Genetics, Harvard Medical School – sequence: 2 givenname: Brandon N. surname: Nicolay fullname: Nicolay, Brandon N. organization: Massachusetts General Hospital Cancer Center – sequence: 3 givenname: Joel M. surname: Chick fullname: Chick, Joel M. organization: Department of Cell Biology, Harvard Medical School – sequence: 4 givenname: Xueliang surname: Gao fullname: Gao, Xueliang organization: Department of Cancer Biology, Dana-Farber Cancer Institute, Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School – sequence: 5 givenname: Yan surname: Geng fullname: Geng, Yan organization: Department of Cancer Biology, Dana-Farber Cancer Institute, Department of Genetics, Harvard Medical School – sequence: 6 givenname: Hong surname: Ren fullname: Ren, Hong organization: Department of Cancer Biology, Dana-Farber Cancer Institute, Department of Genetics, Harvard Medical School – sequence: 7 givenname: Hui surname: Gao fullname: Gao, Hui organization: Novartis Institutes for Biomedical Research – sequence: 8 givenname: Guizhi surname: Yang fullname: Yang, Guizhi organization: Novartis Institutes for Biomedical Research – sequence: 9 givenname: Juliet A. surname: Williams fullname: Williams, Juliet A. organization: Novartis Institutes for Biomedical Research – sequence: 10 givenname: Jan M. surname: Suski fullname: Suski, Jan M. organization: Department of Cancer Biology, Dana-Farber Cancer Institute, Department of Genetics, Harvard Medical School – sequence: 11 givenname: Mark A. surname: Keibler fullname: Keibler, Mark A. organization: Department of Chemical Engineering, Massachusetts Institute of Technology – sequence: 12 givenname: Ewa surname: Sicinska fullname: Sicinska, Ewa organization: Department of Oncologic Pathology, Dana-Farber Cancer Institute – sequence: 13 givenname: Ulrike surname: Gerdemann fullname: Gerdemann, Ulrike organization: Department of Pediatric Oncology, Dana-Farber Cancer Institute – sequence: 14 givenname: W. Nicholas surname: Haining fullname: Haining, W. Nicholas organization: Department of Pediatric Oncology, Dana-Farber Cancer Institute, Division of Pediatric Hematology and Oncology, Children’s Hospital, Broad Institute of MIT and Harvard – sequence: 15 givenname: Thomas M. surname: Roberts fullname: Roberts, Thomas M. organization: Department of Cancer Biology, Dana-Farber Cancer Institute, Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School – sequence: 16 givenname: Kornelia surname: Polyak fullname: Polyak, Kornelia organization: Department of Medical Oncology, Dana-Farber Cancer Institute – sequence: 17 givenname: Steven P. surname: Gygi fullname: Gygi, Steven P. organization: Department of Cell Biology, Harvard Medical School – sequence: 18 givenname: Nicholas J. surname: Dyson fullname: Dyson, Nicholas J. organization: Massachusetts General Hospital Cancer Center – sequence: 19 givenname: Piotr surname: Sicinski fullname: Sicinski, Piotr email: peter_sicinski@dfci.harvard.edu organization: Department of Cancer Biology, Dana-Farber Cancer Institute, Department of Genetics, Harvard Medical School |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28607489$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1126/science.1222278 10.1101/gad.206227.112 10.1016/j.cell.2010.12.001 10.1016/j.gde.2009.01.002 10.1002/nbm.2787 10.1371/journal.pone.0056037 10.1530/rep.0.1240675 10.1038/nm.3954 10.1016/j.ccr.2012.09.016 10.1038/nrc2981 10.1074/jbc.M706494200 10.1016/j.ccr.2012.09.015 10.1016/j.jmb.2011.01.019 10.1038/nature13236 10.1074/jbc.271.30.17875 10.1186/gb4184 10.1016/j.biocel.2010.02.005 10.1016/j.ccr.2010.05.025 10.4161/cc.21195 10.1038/nmeth1019 10.1074/jbc.M112.347153 10.1515/hsz-2013-0130 10.1158/2159-8290.CD-15-0894 10.1016/j.ymben.2006.01.004 10.1016/S0076-6879(82)90107-0 10.1002/bit.21632 10.1038/nbt1240 10.1038/onc.2010.154 10.1038/nature11540 10.1038/nature06734 10.1016/j.ymben.2006.09.001 10.1126/science.1211485 10.1016/S0014-5793(00)01950-5 10.1016/1044-0305(94)80016-2 10.1038/sj.onc.1208618 10.1016/S0021-9258(19)38635-1 |
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| References | Christofk (CR10) 2008; 452 Puyol (CR5) 2010; 18 Yi (CR19) 2012; 337 Cetica, Pintos, Dalvit, Beconi (CR23) 2002; 124 Young, Walther, Antoniewicz, Yoo, Stephanopoulos (CR30) 2008; 99 Nicolay (CR26) 2013; 27 Phong (CR21) 2013; 8 Sawai (CR8) 2012; 22 Marin-Valencia (CR31) 2012; 25 Eng, McCormack, Yates (CR33) 1994; 5 Boada (CR17) 2000; 480 Beausoleil, Villén, Gerber, Rush, Gygi (CR35) 2006; 24 Divita, Goody, Gautheron, Di Pietro (CR24) 1993; 268 Chaneton (CR18) 2012; 491 Schöneberg, Kloos, Brüser, Kirchberger, Sträter (CR14) 2013; 394 Dean, Thangavel, McClendon, Reed, Knudsen (CR4) 2010; 29 Dean (CR6) 2012; 11 Sherr, Beach, Shapiro (CR2) 2016; 6 Kotlarz, Buc (CR22) 1982; 90 Antoniewicz, Kelleher, Stephanopoulos (CR28) 2007; 9 Elias, Gygi (CR34) 2007; 4 Banaszak (CR12) 2011; 407 Brüser, Kirchberger, Kloos, Sträter, Schöneberg (CR13) 2012; 287 Fan (CR20) 2014; 510 Vertommen (CR25) 1996; 271 Deshpande, Sicinski, Hinds (CR3) 2005; 24 Cairns, Harris, Mak (CR9) 2011; 11 Tong, Zhao, Thompson (CR11) 2009; 19 Huttlin (CR32) 2010; 143 Antoniewicz, Kelleher, Stephanopoulos (CR27) 2006; 8 Choi (CR7) 2012; 22 Mazurek (CR15) 2011; 43 Anastasiou (CR16) 2011; 334 Yoo, Antoniewicz, Stephanopoulos, Kelleher (CR29) 2008; 283 Malumbres (CR1) 2014; 15 Gao (CR36) 2015; 21 HR Christofk (BFnature22797_CR10) 2008; 452 H Yoo (BFnature22797_CR29) 2008; 283 JK Eng (BFnature22797_CR33) 1994; 5 S Mazurek (BFnature22797_CR15) 2011; 43 G Divita (BFnature22797_CR24) 1993; 268 JD Young (BFnature22797_CR30) 2008; 99 JE Elias (BFnature22797_CR34) 2007; 4 M Malumbres (BFnature22797_CR1) 2014; 15 W Yi (BFnature22797_CR19) 2012; 337 D Anastasiou (BFnature22797_CR16) 2011; 334 EL Huttlin (BFnature22797_CR32) 2010; 143 A Brüser (BFnature22797_CR13) 2012; 287 BN Nicolay (BFnature22797_CR26) 2013; 27 H Gao (BFnature22797_CR36) 2015; 21 CJ Sherr (BFnature22797_CR2) 2016; 6 P Cetica (BFnature22797_CR23) 2002; 124 JL Dean (BFnature22797_CR6) 2012; 11 J Boada (BFnature22797_CR17) 2000; 480 MR Antoniewicz (BFnature22797_CR28) 2007; 9 JL Dean (BFnature22797_CR4) 2010; 29 I Marin-Valencia (BFnature22797_CR31) 2012; 25 A Deshpande (BFnature22797_CR3) 2005; 24 K Banaszak (BFnature22797_CR12) 2011; 407 YJ Choi (BFnature22797_CR7) 2012; 22 WY Phong (BFnature22797_CR21) 2013; 8 X Tong (BFnature22797_CR11) 2009; 19 MR Antoniewicz (BFnature22797_CR27) 2006; 8 T Schöneberg (BFnature22797_CR14) 2013; 394 M Puyol (BFnature22797_CR5) 2010; 18 B Chaneton (BFnature22797_CR18) 2012; 491 D Vertommen (BFnature22797_CR25) 1996; 271 CM Sawai (BFnature22797_CR8) 2012; 22 RA Cairns (BFnature22797_CR9) 2011; 11 SA Beausoleil (BFnature22797_CR35) 2006; 24 J Fan (BFnature22797_CR20) 2014; 510 D Kotlarz (BFnature22797_CR22) 1982; 90 23064226 - Nature. 2012 Nov 15;491(7424):458-462 8514756 - J Biol Chem. 1993 Jun 25;268(18):13178-86 28607481 - Nature. 2017 Jun 15;546(7658):357-358 17787013 - Biotechnol Bioeng. 2008 Feb 15;99(3):686-99 6218375 - Methods Enzymol. 1982;90 Pt E:60-70 16631402 - Metab Eng. 2006 Jul;8(4):324-37 20473330 - Oncogene. 2010 Jul 15;29(28):4018-32 20156581 - Int J Biochem Cell Biol. 2011 Jul;43(7):969-80 16964243 - Nat Biotechnol. 2006 Oct;24(10):1285-92 22052977 - Science. 2011 Dec 2;334(6060):1278-83 23079656 - Cancer Cell. 2012 Oct 16;22(4):452-65 23729568 - Biol Chem. 2013 Aug;394(8):977-93 22474333 - J Biol Chem. 2012 May 18;287(21):17546-53 24226387 - J Am Soc Mass Spectrom. 1994 Nov;5(11):976-89 17088092 - Metab Eng. 2007 Jan;9(1):68-86 21258394 - Nat Rev Cancer. 2011 Feb;11(2):85-95 15838524 - Oncogene. 2005 Apr 18;24(17):2909-15 25180339 - Genome Biol. 2014;15(6):122 23409118 - PLoS One. 2013;8(2):e56037 18337823 - Nature. 2008 Mar 13;452(7184):230-3 21183079 - Cell. 2010 Dec 23;143(7):1174-89 26658964 - Cancer Discov. 2016 Apr;6(4):353-67 19201187 - Curr Opin Genet Dev. 2009 Feb;19(1):32-7 21241708 - J Mol Biol. 2011 Mar 25;407(2):284-97 23079655 - Cancer Cell. 2012 Oct 16;22(4):438-51 20609353 - Cancer Cell. 2010 Jul 13;18(1):63-73 26479923 - Nat Med. 2015 Nov;21(11):1318-25 18364355 - J Biol Chem. 2008 Jul 25;283(30):20621-7 12417006 - Reproduction. 2002 Nov;124(5):675-81 11034341 - FEBS Lett. 2000 Sep 1;480(2-3):261-4 17327847 - Nat Methods. 2007 Mar;4(3):207-14 8663445 - J Biol Chem. 1996 Jul 26;271(30):17875-80 23322302 - Genes Dev. 2013 Jan 15;27(2):182-96 22923583 - Science. 2012 Aug 24;337(6097):975-80 22383401 - NMR Biomed. 2012 Oct;25(10 ):1177-86 24805240 - Nature. 2014 Jun 12;510(7504):298-302 22767154 - Cell Cycle. 2012 Jul 15;11(14):2756-61 |
| References_xml | – volume: 337 start-page: 975 year: 2012 end-page: 980 ident: CR19 article-title: Phosphofructokinase 1 glycosylation regulates cell growth and metabolism publication-title: Science doi: 10.1126/science.1222278 – volume: 27 start-page: 182 year: 2013 end-page: 196 ident: CR26 article-title: Loss of RBF1 changes glutamine catabolism publication-title: Genes Dev. doi: 10.1101/gad.206227.112 – volume: 143 start-page: 1174 year: 2010 end-page: 1189 ident: CR32 article-title: A tissue-specific atlas of mouse protein phosphorylation and expression publication-title: Cell doi: 10.1016/j.cell.2010.12.001 – volume: 19 start-page: 32 year: 2009 end-page: 37 ident: CR11 article-title: The molecular determinants of de novo nucleotide biosynthesis in cancer cells publication-title: Curr. Opin. Genet. Dev. doi: 10.1016/j.gde.2009.01.002 – volume: 25 start-page: 1177 year: 2012 end-page: 1186 ident: CR31 article-title: Glucose metabolism via the pentose phosphate pathway, glycolysis and Krebs cycle in an orthotopic mouse model of human brain tumors publication-title: NMR Biomed. doi: 10.1002/nbm.2787 – volume: 8 start-page: e56037 year: 2013 ident: CR21 article-title: Characterization of phosphofructokinase activity in reveals that a functional glycolytic carbon flow is necessary to limit the accumulation of toxic metabolic intermediates under hypoxia publication-title: PLoS One doi: 10.1371/journal.pone.0056037 – volume: 124 start-page: 675 year: 2002 end-page: 681 ident: CR23 article-title: Activity of key enzymes involved in glucose and triglyceride catabolism during bovine oocyte maturation in vitro publication-title: Reproduction doi: 10.1530/rep.0.1240675 – volume: 21 start-page: 1318 year: 2015 end-page: 1325 ident: CR36 article-title: High-throughput screening using patient-derived tumor xenografts to predict clinical trial drug response publication-title: Nat. Med. doi: 10.1038/nm.3954 – volume: 268 start-page: 13178 year: 1993 end-page: 13186 ident: CR24 article-title: Structural mapping of catalytic site with respect to alpha-subunit and noncatalytic site in yeast mitochondrial F1-ATPase using fluorescence resonance energy transfer publication-title: J. Biol. Chem. – volume: 22 start-page: 452 year: 2012 end-page: 465 ident: CR8 article-title: Therapeutic targeting of the cyclin D3:CDK4/6 complex in T cell leukemia publication-title: Cancer Cell doi: 10.1016/j.ccr.2012.09.016 – volume: 11 start-page: 85 year: 2011 end-page: 95 ident: CR9 article-title: Regulation of cancer cell metabolism publication-title: Nat. Rev. Cancer doi: 10.1038/nrc2981 – volume: 283 start-page: 20621 year: 2008 end-page: 20627 ident: CR29 article-title: Quantifying reductive carboxylation flux of glutamine to lipid in a brown adipocyte cell line publication-title: J. Biol. Chem. doi: 10.1074/jbc.M706494200 – volume: 22 start-page: 438 year: 2012 end-page: 451 ident: CR7 article-title: The requirement for cyclin D function in tumor maintenance publication-title: Cancer Cell doi: 10.1016/j.ccr.2012.09.015 – volume: 407 start-page: 284 year: 2011 end-page: 297 ident: CR12 article-title: The crystal structures of eukaryotic phosphofructokinases from baker’s yeast and rabbit skeletal muscle publication-title: J. Mol. Biol. doi: 10.1016/j.jmb.2011.01.019 – volume: 510 start-page: 298 year: 2014 end-page: 302 ident: CR20 article-title: Quantitative flux analysis reveals folate-dependent NADPH production publication-title: Nature doi: 10.1038/nature13236 – volume: 271 start-page: 17875 year: 1996 end-page: 17880 ident: CR25 article-title: The ATP-binding site in the 2-kinase domain of liver 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase. Study of the role of Lys-54 and Thr-55 by site-directed mutagenesis publication-title: J. Biol. Chem. doi: 10.1074/jbc.271.30.17875 – volume: 15 start-page: 122 year: 2014 ident: CR1 article-title: Cyclin-dependent kinases publication-title: Genome Biol. doi: 10.1186/gb4184 – volume: 43 start-page: 969 year: 2011 end-page: 980 ident: CR15 article-title: Pyruvate kinase type M2: a key regulator of the metabolic budget system in tumor cells publication-title: Int. J. Biochem. Cell Biol. doi: 10.1016/j.biocel.2010.02.005 – volume: 18 start-page: 63 year: 2010 end-page: 73 ident: CR5 article-title: A synthetic lethal interaction between K-Ras oncogenes and Cdk4 unveils a therapeutic strategy for non-small cell lung carcinoma publication-title: Cancer Cell doi: 10.1016/j.ccr.2010.05.025 – volume: 11 start-page: 2756 year: 2012 end-page: 2761 ident: CR6 article-title: Therapeutic response to CDK4/6 inhibition in breast cancer defined by analyses of human tumors publication-title: Cell Cycle doi: 10.4161/cc.21195 – volume: 4 start-page: 207 year: 2007 end-page: 214 ident: CR34 article-title: Target-decoy search strategy for increased confidence in large-scale protein identifications by mass spectrometry publication-title: Nat. Methods doi: 10.1038/nmeth1019 – volume: 287 start-page: 17546 year: 2012 end-page: 17553 ident: CR13 article-title: Functional linkage of adenine nucleotide binding sites in mammalian muscle 6-phosphofructokinase publication-title: J. Biol. Chem. doi: 10.1074/jbc.M112.347153 – volume: 394 start-page: 977 year: 2013 end-page: 993 ident: CR14 article-title: Structure and allosteric regulation of eukaryotic 6-phosphofructokinases publication-title: Biol. Chem. doi: 10.1515/hsz-2013-0130 – volume: 6 start-page: 353 year: 2016 end-page: 367 ident: CR2 article-title: Targeting CDK4 and CDK6: from discovery to therapy publication-title: Cancer Discov. doi: 10.1158/2159-8290.CD-15-0894 – volume: 8 start-page: 324 year: 2006 end-page: 337 ident: CR27 article-title: Determination of confidence intervals of metabolic fluxes estimated from stable isotope measurements publication-title: Metab. Eng. doi: 10.1016/j.ymben.2006.01.004 – volume: 90 start-page: 60 year: 1982 end-page: 70 ident: CR22 article-title: Phosphofructokinases from publication-title: Methods Enzymol. doi: 10.1016/S0076-6879(82)90107-0 – volume: 99 start-page: 686 year: 2008 end-page: 699 ident: CR30 article-title: An elementary metabolite unit (EMU) based method of isotopically nonstationary flux analysis publication-title: Biotechnol. Bioeng. doi: 10.1002/bit.21632 – volume: 24 start-page: 1285 year: 2006 end-page: 1292 ident: CR35 article-title: A probability-based approach for high-throughput protein phosphorylation analysis and site localization publication-title: Nat. Biotechnol. doi: 10.1038/nbt1240 – volume: 29 start-page: 4018 year: 2010 end-page: 4032 ident: CR4 article-title: Therapeutic CDK4/6 inhibition in breast cancer: key mechanisms of response and failure publication-title: Oncogene doi: 10.1038/onc.2010.154 – volume: 491 start-page: 458 year: 2012 end-page: 462 ident: CR18 article-title: Serine is a natural ligand and allosteric activator of pyruvate kinase M2 publication-title: Nature doi: 10.1038/nature11540 – volume: 452 start-page: 230 year: 2008 end-page: 233 ident: CR10 article-title: The M2 splice isoform of pyruvate kinase is important for cancer metabolism and tumour growth publication-title: Nature doi: 10.1038/nature06734 – volume: 9 start-page: 68 year: 2007 end-page: 86 ident: CR28 article-title: Elementary metabolite units (EMU): a novel framework for modeling isotopic distributions publication-title: Metab. Eng. doi: 10.1016/j.ymben.2006.09.001 – volume: 334 start-page: 1278 year: 2011 end-page: 1283 ident: CR16 article-title: Inhibition of pyruvate kinase M2 by reactive oxygen species contributes to cellular antioxidant responses publication-title: Science doi: 10.1126/science.1211485 – volume: 480 start-page: 261 year: 2000 end-page: 264 ident: CR17 article-title: Cells overexpressing fructose-2,6-bisphosphatase showed enhanced pentose phosphate pathway flux and resistance to oxidative stress publication-title: FEBS Lett. doi: 10.1016/S0014-5793(00)01950-5 – volume: 5 start-page: 976 year: 1994 end-page: 989 ident: CR33 article-title: An approach to correlate tandem mass spectral data of peptides with amino acid sequences in a protein database publication-title: J. Am. Soc. Mass Spectrom. doi: 10.1016/1044-0305(94)80016-2 – volume: 24 start-page: 2909 year: 2005 end-page: 2915 ident: CR3 article-title: Cyclins and CDKs in development and cancer: a perspective publication-title: Oncogene doi: 10.1038/sj.onc.1208618 – volume: 99 start-page: 686 year: 2008 ident: BFnature22797_CR30 publication-title: Biotechnol. Bioeng. doi: 10.1002/bit.21632 – volume: 8 start-page: 324 year: 2006 ident: BFnature22797_CR27 publication-title: Metab. Eng. doi: 10.1016/j.ymben.2006.01.004 – volume: 29 start-page: 4018 year: 2010 ident: BFnature22797_CR4 publication-title: Oncogene doi: 10.1038/onc.2010.154 – volume: 18 start-page: 63 year: 2010 ident: BFnature22797_CR5 publication-title: Cancer Cell doi: 10.1016/j.ccr.2010.05.025 – volume: 43 start-page: 969 year: 2011 ident: BFnature22797_CR15 publication-title: Int. J. Biochem. Cell Biol. doi: 10.1016/j.biocel.2010.02.005 – volume: 334 start-page: 1278 year: 2011 ident: BFnature22797_CR16 publication-title: Science doi: 10.1126/science.1211485 – volume: 11 start-page: 2756 year: 2012 ident: BFnature22797_CR6 publication-title: Cell Cycle doi: 10.4161/cc.21195 – volume: 21 start-page: 1318 year: 2015 ident: BFnature22797_CR36 publication-title: Nat. Med. doi: 10.1038/nm.3954 – volume: 510 start-page: 298 year: 2014 ident: BFnature22797_CR20 publication-title: Nature doi: 10.1038/nature13236 – volume: 25 start-page: 1177 year: 2012 ident: BFnature22797_CR31 publication-title: NMR Biomed. doi: 10.1002/nbm.2787 – volume: 287 start-page: 17546 year: 2012 ident: BFnature22797_CR13 publication-title: J. Biol. Chem. doi: 10.1074/jbc.M112.347153 – volume: 27 start-page: 182 year: 2013 ident: BFnature22797_CR26 publication-title: Genes Dev. doi: 10.1101/gad.206227.112 – volume: 491 start-page: 458 year: 2012 ident: BFnature22797_CR18 publication-title: Nature doi: 10.1038/nature11540 – volume: 11 start-page: 85 year: 2011 ident: BFnature22797_CR9 publication-title: Nat. Rev. Cancer doi: 10.1038/nrc2981 – volume: 452 start-page: 230 year: 2008 ident: BFnature22797_CR10 publication-title: Nature doi: 10.1038/nature06734 – volume: 268 start-page: 13178 year: 1993 ident: BFnature22797_CR24 publication-title: J. Biol. Chem. doi: 10.1016/S0021-9258(19)38635-1 – volume: 337 start-page: 975 year: 2012 ident: BFnature22797_CR19 publication-title: Science doi: 10.1126/science.1222278 – volume: 4 start-page: 207 year: 2007 ident: BFnature22797_CR34 publication-title: Nat. Methods doi: 10.1038/nmeth1019 – volume: 22 start-page: 452 year: 2012 ident: BFnature22797_CR8 publication-title: Cancer Cell doi: 10.1016/j.ccr.2012.09.016 – volume: 22 start-page: 438 year: 2012 ident: BFnature22797_CR7 publication-title: Cancer Cell doi: 10.1016/j.ccr.2012.09.015 – volume: 24 start-page: 1285 year: 2006 ident: BFnature22797_CR35 publication-title: Nat. Biotechnol. doi: 10.1038/nbt1240 – volume: 283 start-page: 20621 year: 2008 ident: BFnature22797_CR29 publication-title: J. Biol. Chem. doi: 10.1074/jbc.M706494200 – volume: 19 start-page: 32 year: 2009 ident: BFnature22797_CR11 publication-title: Curr. Opin. Genet. Dev. doi: 10.1016/j.gde.2009.01.002 – volume: 5 start-page: 976 year: 1994 ident: BFnature22797_CR33 publication-title: J. Am. Soc. Mass Spectrom. doi: 10.1016/1044-0305(94)80016-2 – volume: 90 start-page: 60 year: 1982 ident: BFnature22797_CR22 publication-title: Methods Enzymol. doi: 10.1016/S0076-6879(82)90107-0 – volume: 271 start-page: 17875 year: 1996 ident: BFnature22797_CR25 publication-title: J. Biol. Chem. doi: 10.1074/jbc.271.30.17875 – volume: 8 start-page: e56037 year: 2013 ident: BFnature22797_CR21 publication-title: PLoS One doi: 10.1371/journal.pone.0056037 – volume: 143 start-page: 1174 year: 2010 ident: BFnature22797_CR32 publication-title: Cell doi: 10.1016/j.cell.2010.12.001 – volume: 24 start-page: 2909 year: 2005 ident: BFnature22797_CR3 publication-title: Oncogene doi: 10.1038/sj.onc.1208618 – volume: 394 start-page: 977 year: 2013 ident: BFnature22797_CR14 publication-title: Biol. Chem. doi: 10.1515/hsz-2013-0130 – volume: 6 start-page: 353 year: 2016 ident: BFnature22797_CR2 publication-title: Cancer Discov. doi: 10.1158/2159-8290.CD-15-0894 – volume: 407 start-page: 284 year: 2011 ident: BFnature22797_CR12 publication-title: J. Mol. Biol. doi: 10.1016/j.jmb.2011.01.019 – volume: 124 start-page: 675 year: 2002 ident: BFnature22797_CR23 publication-title: Reproduction doi: 10.1530/rep.0.1240675 – volume: 15 start-page: 122 year: 2014 ident: BFnature22797_CR1 publication-title: Genome Biol. doi: 10.1186/gb4184 – volume: 480 start-page: 261 year: 2000 ident: BFnature22797_CR17 publication-title: FEBS Lett. doi: 10.1016/S0014-5793(00)01950-5 – volume: 9 start-page: 68 year: 2007 ident: BFnature22797_CR28 publication-title: Metab. Eng. doi: 10.1016/j.ymben.2006.09.001 – reference: 20156581 - Int J Biochem Cell Biol. 2011 Jul;43(7):969-80 – reference: 23064226 - Nature. 2012 Nov 15;491(7424):458-462 – reference: 26658964 - Cancer Discov. 2016 Apr;6(4):353-67 – reference: 6218375 - Methods Enzymol. 1982;90 Pt E:60-70 – reference: 22383401 - NMR Biomed. 2012 Oct;25(10 ):1177-86 – reference: 23079656 - Cancer Cell. 2012 Oct 16;22(4):452-65 – reference: 20473330 - Oncogene. 2010 Jul 15;29(28):4018-32 – reference: 22767154 - Cell Cycle. 2012 Jul 15;11(14):2756-61 – reference: 12417006 - Reproduction. 2002 Nov;124(5):675-81 – reference: 17088092 - Metab Eng. 2007 Jan;9(1):68-86 – reference: 18364355 - J Biol Chem. 2008 Jul 25;283(30):20621-7 – reference: 23729568 - Biol Chem. 2013 Aug;394(8):977-93 – reference: 18337823 - Nature. 2008 Mar 13;452(7184):230-3 – reference: 8514756 - J Biol Chem. 1993 Jun 25;268(18):13178-86 – reference: 19201187 - Curr Opin Genet Dev. 2009 Feb;19(1):32-7 – reference: 20609353 - Cancer Cell. 2010 Jul 13;18(1):63-73 – reference: 22474333 - J Biol Chem. 2012 May 18;287(21):17546-53 – reference: 17787013 - Biotechnol Bioeng. 2008 Feb 15;99(3):686-99 – reference: 24805240 - Nature. 2014 Jun 12;510(7504):298-302 – reference: 21183079 - Cell. 2010 Dec 23;143(7):1174-89 – reference: 17327847 - Nat Methods. 2007 Mar;4(3):207-14 – reference: 21258394 - Nat Rev Cancer. 2011 Feb;11(2):85-95 – reference: 11034341 - FEBS Lett. 2000 Sep 1;480(2-3):261-4 – reference: 23079655 - Cancer Cell. 2012 Oct 16;22(4):438-51 – reference: 22052977 - Science. 2011 Dec 2;334(6060):1278-83 – reference: 8663445 - J Biol Chem. 1996 Jul 26;271(30):17875-80 – reference: 28607481 - Nature. 2017 Jun 15;546(7658):357-358 – reference: 15838524 - Oncogene. 2005 Apr 18;24(17):2909-15 – reference: 23409118 - PLoS One. 2013;8(2):e56037 – reference: 25180339 - Genome Biol. 2014;15(6):122 – reference: 22923583 - Science. 2012 Aug 24;337(6097):975-80 – reference: 16964243 - Nat Biotechnol. 2006 Oct;24(10):1285-92 – reference: 16631402 - Metab Eng. 2006 Jul;8(4):324-37 – reference: 26479923 - Nat Med. 2015 Nov;21(11):1318-25 – reference: 21241708 - J Mol Biol. 2011 Mar 25;407(2):284-97 – reference: 23322302 - Genes Dev. 2013 Jan 15;27(2):182-96 – reference: 24226387 - J Am Soc Mass Spectrom. 1994 Nov;5(11):976-89 |
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| Snippet | The cyclin D3–CDK6 kinase complex, which is overactive in some cancers, inhibits two key glycolysis enzymes and thereby enhances the levels of antioxidants in... D-type cyclins (D1, D2 and D3) and their associated cyclin-dependent kinases (CDK4 and CDK6) are components of the core cell cycle machinery that drives cell... D-type cyclins (D1, D2 and D3) and their associated cyclindependent kinases (CDK4 and CDK6) are components of the core cell cycle machinery that drives cell... D-type cyclins (D1, D2 and D3) together with their associated cyclin-dependent kinases CDK4 and CDK6 are components of the core cell cycle machinery that... |
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| Title | The metabolic function of cyclin D3–CDK6 kinase in cancer cell survival |
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