Hypoxia regulates the mitochondrial activity of hepatocellular carcinoma cells through HIF/HEY1/PINK1 pathway

Hypoxia is commonly found in cancers. Hypoxia, due to the lack of oxygen (O 2 ) as the electron recipient, causes inefficient electron transfer through the electron transport chain at the mitochondria leading to accumulation of reactive oxygen species (ROS) which could create irreversible cellular d...

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Published inCell death & disease Vol. 10; no. 12; pp. 934 - 16
Main Authors Kung-Chun Chiu, David, Pui-Wah Tse, Aki, Law, Cheuk-Ting, Ming-Jing Xu, Iris, Lee, Derek, Chen, Mengnuo, Kit-Ho Lai, Robin, Wai-Hin Yuen, Vincent, Wing-Sum Cheu, Jacinth, Wai-Hung Ho, Daniel, Wong, Chun-Ming, Zhang, Huafeng, Ng, Irene Oi-Lin, Chak-Lui Wong, Carmen
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 09.12.2019
Springer Nature B.V
Subjects
13
13/1
13/106
13/109
13/31
13/51
14
14/28
38
631/67/2327
631/80/86/2366
Animals
Antibodies
Basic Helix-Loop-Helix Transcription Factors - genetics
Basic Helix-Loop-Helix Transcription Factors - metabolism
Biochemistry
Biomedical and Life Sciences
Biosynthesis
Carcinoma, Hepatocellular - metabolism
Carcinoma, Hepatocellular - pathology
Cell Biology
Cell Culture
Cell Cycle Proteins - genetics
Cell Cycle Proteins - metabolism
Cell Hypoxia - genetics
Chromatin
Cristae
Electron transfer
Electron transport chain
Gene expression
HeLa Cells
Hep G2 Cells
Hepatocellular carcinoma
Heterografts
Humans
Hypoxia
Hypoxia-inducible factor 1
Hypoxia-Inducible Factor 1, alpha Subunit - genetics
Hypoxia-Inducible Factor 1, alpha Subunit - metabolism
Hypoxia-inducible factors
Immunology
Immunoprecipitation
Life Sciences
Liver cancer
Liver Neoplasms - metabolism
Liver Neoplasms - pathology
Male
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Nude
Mitochondria
Mitochondria - metabolism
Molecular modelling
Oxidative stress
Protein Kinases - genetics
Protein Kinases - metabolism
PTEN-induced putative kinase
Reactive oxygen species
Regulatory sequences
Therapeutic applications
Transcription
Transcriptomes
Transfection
Tumor Burden - genetics
Tumors
Online AccessGet full text

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Abstract Hypoxia is commonly found in cancers. Hypoxia, due to the lack of oxygen (O 2 ) as the electron recipient, causes inefficient electron transfer through the electron transport chain at the mitochondria leading to accumulation of reactive oxygen species (ROS) which could create irreversible cellular damages. Through hypoxia-inducible factor 1 (HIF-1) which elicits various molecular events, cells are able to overcome low O 2 . Knowledge about the new molecular mechanisms governed by HIF-1 is important for new therapeutic interventions targeting hypoxic tumors. Using hepatocellular carcinoma (HCC) as a model, we revealed that the HIF-1 and the Notch signaling pathways cross-talk to control mitochondrial biogenesis of cancer cells to maintain REDOX balance. From transcriptome sequencing, we found that HEY1, a transcriptional repressor, in the NOTCH pathway was consistently induced by hypoxia in HCC cell lines. We identified a strong hypoxia response element (HRE) in HEY1 by chromatin immunoprecipitation (ChIP) and luciferase reporter assays. Transcriptome and ChIP sequencing further identified PINK1, a gene essential for mitochondrial biogenesis, as a novel transcriptional target of HEY1. HCC cells with HEY1 knockdown re-expressed PINK1. HEY1 and PINK1 expressions inversely correlated in human HCC samples. Overexpression of HEY1 and under-expression of PINK1 were detected in human HCC and associated with poor clinical outcomes. Functionally, we found that overexpression of HEY1 or knockdown of PINK1 consistently reduced mitochondrial cristae, mitochondrial mass, oxidative stress level, and increased HCC growth.
AbstractList Hypoxia is commonly found in cancers. Hypoxia, due to the lack of oxygen (O2) as the electron recipient, causes inefficient electron transfer through the electron transport chain at the mitochondria leading to accumulation of reactive oxygen species (ROS) which could create irreversible cellular damages. Through hypoxia-inducible factor 1 (HIF-1) which elicits various molecular events, cells are able to overcome low O2. Knowledge about the new molecular mechanisms governed by HIF-1 is important for new therapeutic interventions targeting hypoxic tumors. Using hepatocellular carcinoma (HCC) as a model, we revealed that the HIF-1 and the Notch signaling pathways cross-talk to control mitochondrial biogenesis of cancer cells to maintain REDOX balance. From transcriptome sequencing, we found that HEY1, a transcriptional repressor, in the NOTCH pathway was consistently induced by hypoxia in HCC cell lines. We identified a strong hypoxia response element (HRE) in HEY1 by chromatin immunoprecipitation (ChIP) and luciferase reporter assays. Transcriptome and ChIP sequencing further identified PINK1, a gene essential for mitochondrial biogenesis, as a novel transcriptional target of HEY1. HCC cells with HEY1 knockdown re-expressed PINK1. HEY1 and PINK1 expressions inversely correlated in human HCC samples. Overexpression of HEY1 and under-expression of PINK1 were detected in human HCC and associated with poor clinical outcomes. Functionally, we found that overexpression of HEY1 or knockdown of PINK1 consistently reduced mitochondrial cristae, mitochondrial mass, oxidative stress level, and increased HCC growth.
Hypoxia is commonly found in cancers. Hypoxia, due to the lack of oxygen (O ) as the electron recipient, causes inefficient electron transfer through the electron transport chain at the mitochondria leading to accumulation of reactive oxygen species (ROS) which could create irreversible cellular damages. Through hypoxia-inducible factor 1 (HIF-1) which elicits various molecular events, cells are able to overcome low O . Knowledge about the new molecular mechanisms governed by HIF-1 is important for new therapeutic interventions targeting hypoxic tumors. Using hepatocellular carcinoma (HCC) as a model, we revealed that the HIF-1 and the Notch signaling pathways cross-talk to control mitochondrial biogenesis of cancer cells to maintain REDOX balance. From transcriptome sequencing, we found that HEY1, a transcriptional repressor, in the NOTCH pathway was consistently induced by hypoxia in HCC cell lines. We identified a strong hypoxia response element (HRE) in HEY1 by chromatin immunoprecipitation (ChIP) and luciferase reporter assays. Transcriptome and ChIP sequencing further identified PINK1, a gene essential for mitochondrial biogenesis, as a novel transcriptional target of HEY1. HCC cells with HEY1 knockdown re-expressed PINK1. HEY1 and PINK1 expressions inversely correlated in human HCC samples. Overexpression of HEY1 and under-expression of PINK1 were detected in human HCC and associated with poor clinical outcomes. Functionally, we found that overexpression of HEY1 or knockdown of PINK1 consistently reduced mitochondrial cristae, mitochondrial mass, oxidative stress level, and increased HCC growth.
Hypoxia is commonly found in cancers. Hypoxia, due to the lack of oxygen (O2) as the electron recipient, causes inefficient electron transfer through the electron transport chain at the mitochondria leading to accumulation of reactive oxygen species (ROS) which could create irreversible cellular damages. Through hypoxia-inducible factor 1 (HIF-1) which elicits various molecular events, cells are able to overcome low O2. Knowledge about the new molecular mechanisms governed by HIF-1 is important for new therapeutic interventions targeting hypoxic tumors. Using hepatocellular carcinoma (HCC) as a model, we revealed that the HIF-1 and the Notch signaling pathways cross-talk to control mitochondrial biogenesis of cancer cells to maintain REDOX balance. From transcriptome sequencing, we found that HEY1, a transcriptional repressor, in the NOTCH pathway was consistently induced by hypoxia in HCC cell lines. We identified a strong hypoxia response element (HRE) in HEY1 by chromatin immunoprecipitation (ChIP) and luciferase reporter assays. Transcriptome and ChIP sequencing further identified PINK1, a gene essential for mitochondrial biogenesis, as a novel transcriptional target of HEY1. HCC cells with HEY1 knockdown re-expressed PINK1. HEY1 and PINK1 expressions inversely correlated in human HCC samples. Overexpression of HEY1 and under-expression of PINK1 were detected in human HCC and associated with poor clinical outcomes. Functionally, we found that overexpression of HEY1 or knockdown of PINK1 consistently reduced mitochondrial cristae, mitochondrial mass, oxidative stress level, and increased HCC growth.Hypoxia is commonly found in cancers. Hypoxia, due to the lack of oxygen (O2) as the electron recipient, causes inefficient electron transfer through the electron transport chain at the mitochondria leading to accumulation of reactive oxygen species (ROS) which could create irreversible cellular damages. Through hypoxia-inducible factor 1 (HIF-1) which elicits various molecular events, cells are able to overcome low O2. Knowledge about the new molecular mechanisms governed by HIF-1 is important for new therapeutic interventions targeting hypoxic tumors. Using hepatocellular carcinoma (HCC) as a model, we revealed that the HIF-1 and the Notch signaling pathways cross-talk to control mitochondrial biogenesis of cancer cells to maintain REDOX balance. From transcriptome sequencing, we found that HEY1, a transcriptional repressor, in the NOTCH pathway was consistently induced by hypoxia in HCC cell lines. We identified a strong hypoxia response element (HRE) in HEY1 by chromatin immunoprecipitation (ChIP) and luciferase reporter assays. Transcriptome and ChIP sequencing further identified PINK1, a gene essential for mitochondrial biogenesis, as a novel transcriptional target of HEY1. HCC cells with HEY1 knockdown re-expressed PINK1. HEY1 and PINK1 expressions inversely correlated in human HCC samples. Overexpression of HEY1 and under-expression of PINK1 were detected in human HCC and associated with poor clinical outcomes. Functionally, we found that overexpression of HEY1 or knockdown of PINK1 consistently reduced mitochondrial cristae, mitochondrial mass, oxidative stress level, and increased HCC growth.
Hypoxia is commonly found in cancers. Hypoxia, due to the lack of oxygen (O 2 ) as the electron recipient, causes inefficient electron transfer through the electron transport chain at the mitochondria leading to accumulation of reactive oxygen species (ROS) which could create irreversible cellular damages. Through hypoxia-inducible factor 1 (HIF-1) which elicits various molecular events, cells are able to overcome low O 2 . Knowledge about the new molecular mechanisms governed by HIF-1 is important for new therapeutic interventions targeting hypoxic tumors. Using hepatocellular carcinoma (HCC) as a model, we revealed that the HIF-1 and the Notch signaling pathways cross-talk to control mitochondrial biogenesis of cancer cells to maintain REDOX balance. From transcriptome sequencing, we found that HEY1, a transcriptional repressor, in the NOTCH pathway was consistently induced by hypoxia in HCC cell lines. We identified a strong hypoxia response element (HRE) in HEY1 by chromatin immunoprecipitation (ChIP) and luciferase reporter assays. Transcriptome and ChIP sequencing further identified PINK1, a gene essential for mitochondrial biogenesis, as a novel transcriptional target of HEY1. HCC cells with HEY1 knockdown re-expressed PINK1. HEY1 and PINK1 expressions inversely correlated in human HCC samples. Overexpression of HEY1 and under-expression of PINK1 were detected in human HCC and associated with poor clinical outcomes. Functionally, we found that overexpression of HEY1 or knockdown of PINK1 consistently reduced mitochondrial cristae, mitochondrial mass, oxidative stress level, and increased HCC growth.
Abstract Hypoxia is commonly found in cancers. Hypoxia, due to the lack of oxygen (O 2 ) as the electron recipient, causes inefficient electron transfer through the electron transport chain at the mitochondria leading to accumulation of reactive oxygen species (ROS) which could create irreversible cellular damages. Through hypoxia-inducible factor 1 (HIF-1) which elicits various molecular events, cells are able to overcome low O 2 . Knowledge about the new molecular mechanisms governed by HIF-1 is important for new therapeutic interventions targeting hypoxic tumors. Using hepatocellular carcinoma (HCC) as a model, we revealed that the HIF-1 and the Notch signaling pathways cross-talk to control mitochondrial biogenesis of cancer cells to maintain REDOX balance. From transcriptome sequencing, we found that HEY1, a transcriptional repressor, in the NOTCH pathway was consistently induced by hypoxia in HCC cell lines. We identified a strong hypoxia response element (HRE) in HEY1 by chromatin immunoprecipitation (ChIP) and luciferase reporter assays. Transcriptome and ChIP sequencing further identified PINK1, a gene essential for mitochondrial biogenesis, as a novel transcriptional target of HEY1. HCC cells with HEY1 knockdown re-expressed PINK1. HEY1 and PINK1 expressions inversely correlated in human HCC samples. Overexpression of HEY1 and under-expression of PINK1 were detected in human HCC and associated with poor clinical outcomes. Functionally, we found that overexpression of HEY1 or knockdown of PINK1 consistently reduced mitochondrial cristae, mitochondrial mass, oxidative stress level, and increased HCC growth.
ArticleNumber 934
Author Ming-Jing Xu, Iris
Zhang, Huafeng
Lee, Derek
Kung-Chun Chiu, David
Wai-Hin Yuen, Vincent
Chen, Mengnuo
Wing-Sum Cheu, Jacinth
Wong, Chun-Ming
Chak-Lui Wong, Carmen
Wai-Hung Ho, Daniel
Kit-Ho Lai, Robin
Law, Cheuk-Ting
Pui-Wah Tse, Aki
Ng, Irene Oi-Lin
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/31819034$$D View this record in MEDLINE/PubMed
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Cites_doi 10.1056/NEJMoa0708857
10.1016/j.cmet.2006.02.002
10.1002/hep.30467
10.1038/srep27411
10.1073/pnas.92.12.5510
10.1038/nri.2016.93
10.1101/gad.12.2.149
10.1073/pnas.0913485107
10.1038/sj.onc.1204608
10.1038/srep06962
10.1007/s11684-013-0301-3
10.1002/humu.20719
10.1073/pnas.1113483108
10.1158/1078-0432.CCR-15-1987
10.1038/nbt.1621
10.1038/nrm2009
10.1038/ng.2529
10.1016/j.molcel.2009.02.013
10.1016/j.cell.2007.01.047
10.1083/jcb.201509003
10.1158/0008-5472.CAN-15-3079
10.1016/S0140-6736(17)31046-2
10.1038/ncomms5514
10.1016/j.ccr.2006.04.023
10.1089/scd.2014.0471
10.1038/ncb2901
10.1016/j.celrep.2016.04.019
10.1172/JCI90253
10.1038/aps.2015.71
10.1016/S0021-9258(17)31580-6
10.1016/S1470-2045(08)70285-7
10.1126/science.1249161
10.1074/jbc.271.51.32529
10.1038/cdd.2013.19
10.1016/S0092-8674(01)00507-4
10.1152/physrev.00022.2010
10.1074/jbc.M114.620906
10.1038/nature14136
10.1074/jbc.M800102200
10.1016/j.cell.2012.01.021
10.1016/j.ccr.2007.04.001
10.1073/pnas.0901104106
10.1073/pnas.1508779113
10.1158/0008-5472.CAN-07-2095
10.1016/j.devcel.2005.09.010
10.1038/ncb1644
10.1002/1097-0142(19951215)76:12<2443::AID-CNCR2820761207>3.0.CO;2-F
10.1016/j.cmet.2011.10.008
10.1371/journal.pgen.1002728
10.1128/MCB.00440-07
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2019. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
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References Bagchi, Mills (CR47) 2008; 68
Qiu (CR21) 2016; 6
Requejo-Aguilar (CR45) 2014; 5
Unoki, Nakamura (CR51) 2001; 20
Semenza (CR14) 1996; 271
Lee (CR29) 2019; 69
Morais (CR36) 2014; 344
Tufi (CR46) 2014; 16
Wang, Ding, Meng (CR33) 2015; 36
Fantin, St-Pierre, Leder (CR13) 2006; 9
Bray (CR18) 2006; 7
Mei (CR50) 2009; 106
Corti, Lesage, Brice (CR34) 2011; 91
Epstein (CR7) 2001; 107
Marongiu (CR35) 2008; 29
Semenza, Roth, Fang, Wang (CR11) 1994; 269
Zhang (CR17) 2007; 11
Semenza (CR6) 2012; 148
CR3
Konermann (CR24) 2015; 517
Cakouros (CR31) 2015; 24
Zhang (CR44) 2008; 283
El-Khoueiry, Sangro, Yau, Crocenzi, Kudo, Hsu, Kim, Choo, Trojan, Welling, Meyer, Kang, Yeo, Chopra, Anderson, dela Cruz, Lang, Neely, Tang, Dastani, Melero (CR4) 2017; 389
Cheng (CR1) 2009; 10
Agnihotri (CR48) 2016; 76
Ziviani, Tao, Whitworth (CR43) 2010; 107
Arena (CR37) 2013; 20
Pryde, Smith, Chau, Schapira (CR41) 2016; 213
Wong, Kai, Ng (CR5) 2013; 8
Wang, Jiang, Rue, Semenza (CR8) 1995; 92
Aerts, Craessaerts, De Strooper, Morais (CR40) 2015; 290
Lee (CR28) 2017; 127
Lai (CR23) 2016; 22
Pugh (CR49) 2013; 45
Gandhi (CR39) 2009; 33
Lau (CR19) 2016; 15
Kim, Gao, Liu, Semenza, Dang (CR10) 2007; 27
Fukuda (CR15) 2007; 129
Iyer (CR9) 1998; 12
Tsai (CR42) 2014; 4
Xu (CR30) 2016; 113
Kim, Tchernyshyov, Semenza, Dang (CR12) 2006; 3
Wong (CR22) 2011; 108
Ng, Lai, Fan, Ng, So (CR26) 1995; 76
Llovet (CR2) 2008; 359
Tello (CR16) 2011; 14
Gustafsson (CR20) 2005; 9
Trapnell (CR25) 2010; 28
Lucas, Chandra, Nejentsev, Condliffe, Okkenhaug (CR32) 2016; 16
Plun-Favreau (CR38) 2007; 9
Heisig (CR27) 2012; 8
D Lee (2155_CR28) 2017; 127
JW Kim (2155_CR12) 2006; 3
GL Semenza (2155_CR11) 1994; 269
GL Semenza (2155_CR14) 1996; 271
S Agnihotri (2155_CR48) 2016; 76
Y Mei (2155_CR50) 2009; 106
H Zhang (2155_CR17) 2007; 11
2155_CR3
Z Qiu (2155_CR21) 2016; 6
AL Cheng (2155_CR1) 2009; 10
AC Epstein (2155_CR7) 2001; 107
IO Ng (2155_CR26) 1995; 76
L Aerts (2155_CR40) 2015; 290
GL Wang (2155_CR8) 1995; 92
CL Lucas (2155_CR32) 2016; 16
R Fukuda (2155_CR15) 2007; 129
X Wang (2155_CR33) 2015; 36
D Lee (2155_CR29) 2019; 69
E Ziviani (2155_CR43) 2010; 107
D Cakouros (2155_CR31) 2015; 24
R Marongiu (2155_CR35) 2008; 29
O Corti (2155_CR34) 2011; 91
R Tufi (2155_CR46) 2014; 16
CC Wong (2155_CR22) 2011; 108
Carmen Chak-Lui Wong (2155_CR5) 2013; 8
A Bagchi (2155_CR47) 2008; 68
TJ Pugh (2155_CR49) 2013; 45
Anthony B El-Khoueiry (2155_CR4) 2017; 389
GL Semenza (2155_CR6) 2012; 148
VR Fantin (2155_CR13) 2006; 9
RK Lai (2155_CR23) 2016; 22
S Gandhi (2155_CR39) 2009; 33
G Arena (2155_CR37) 2013; 20
D Tello (2155_CR16) 2011; 14
KR Pryde (2155_CR41) 2016; 213
JM Llovet (2155_CR2) 2008; 359
PI Tsai (2155_CR42) 2014; 4
Gustafsson (2155_CR20) 2005; 9
SJ Bray (2155_CR18) 2006; 7
NV Iyer (2155_CR9) 1998; 12
S Konermann (2155_CR24) 2015; 517
H Zhang (2155_CR44) 2008; 283
M Unoki (2155_CR51) 2001; 20
JW Kim (2155_CR10) 2007; 27
C Trapnell (2155_CR25) 2010; 28
H Plun-Favreau (2155_CR38) 2007; 9
EY Lau (2155_CR19) 2016; 15
R Requejo-Aguilar (2155_CR45) 2014; 5
J Heisig (2155_CR27) 2012; 8
IM Xu (2155_CR30) 2016; 113
VA Morais (2155_CR36) 2014; 344
References_xml – volume: 359
  start-page: 378
  year: 2008
  end-page: 390
  ident: CR2
  article-title: Sorafenib in advanced hepatocellular carcinoma
  publication-title: N. Engl. J. Med.
  doi: 10.1056/NEJMoa0708857
  contributor:
    fullname: Llovet
– volume: 3
  start-page: 177
  year: 2006
  end-page: 185
  ident: CR12
  article-title: HIF-1-mediated expression of pyruvate dehydrogenase kinase: a metabolic switch required for cellular adaptation to hypoxia
  publication-title: Cell Metab.
  doi: 10.1016/j.cmet.2006.02.002
  contributor:
    fullname: Dang
– volume: 69
  start-page: 1768
  year: 2019
  end-page: 1786
  ident: CR29
  article-title: Induction of oxidative stress through inhibition of thioredoxin reductase 1 is an effective therapeutic approach for hepatocellular carcinoma
  publication-title: Hepatology
  doi: 10.1002/hep.30467
  contributor:
    fullname: Lee
– volume: 6
  year: 2016
  ident: CR21
  article-title: Hepatocellular carcinoma cell lines retain the genomic and transcriptomic landscapes of primary human cancers
  publication-title: Sci. Rep.
  doi: 10.1038/srep27411
  contributor:
    fullname: Qiu
– volume: 92
  start-page: 5510
  year: 1995
  end-page: 5514
  ident: CR8
  article-title: Hypoxia-inducible factor 1 is a basic-helix-loop-helix-PAS heterodimer regulated by cellular O2 tension
  publication-title: Proc. Natl Acad. Sci. USA
  doi: 10.1073/pnas.92.12.5510
  contributor:
    fullname: Semenza
– volume: 16
  start-page: 702
  year: 2016
  end-page: 714
  ident: CR32
  article-title: PI3Kdelta and primary immunodeficiencies
  publication-title: Nat. Rev. Immunol.
  doi: 10.1038/nri.2016.93
  contributor:
    fullname: Okkenhaug
– volume: 12
  start-page: 149
  year: 1998
  end-page: 162
  ident: CR9
  article-title: Cellular and developmental control of O2 homeostasis by hypoxia-inducible factor 1 alpha
  publication-title: Genes Dev.
  doi: 10.1101/gad.12.2.149
  contributor:
    fullname: Iyer
– volume: 107
  start-page: 5018
  year: 2010
  end-page: 5023
  ident: CR43
  article-title: Drosophila parkin requires PINK1 for mitochondrial translocation and ubiquitinates mitofusin
  publication-title: Proc. Natl Acad. Sci. USA
  doi: 10.1073/pnas.0913485107
  contributor:
    fullname: Whitworth
– volume: 20
  start-page: 4457
  year: 2001
  end-page: 4465
  ident: CR51
  article-title: Growth-suppressive effects of BPOZ and EGR2, two genes involved in the PTEN signaling pathway
  publication-title: Oncogene
  doi: 10.1038/sj.onc.1204608
  contributor:
    fullname: Nakamura
– volume: 4
  year: 2014
  ident: CR42
  article-title: PINK1-mediated phosphorylation of Miro inhibits synaptic growth and protects dopaminergic neurons in Drosophila
  publication-title: Sci. Rep.
  doi: 10.1038/srep06962
  contributor:
    fullname: Tsai
– volume: 8
  start-page: 33
  issue: 1
  year: 2013
  end-page: 41
  ident: CR5
  article-title: The impact of hypoxia in hepatocellular carcinoma metastasis
  publication-title: Frontiers of Medicine
  doi: 10.1007/s11684-013-0301-3
  contributor:
    fullname: Ng
– volume: 29
  start-page: 565
  year: 2008
  ident: CR35
  article-title: PINK1 heterozygous rare variants: prevalence, significance and phenotypic spectrum
  publication-title: Hum. Mutat.
  doi: 10.1002/humu.20719
  contributor:
    fullname: Marongiu
– volume: 108
  start-page: 16369
  year: 2011
  end-page: 16374
  ident: CR22
  article-title: Hypoxia-inducible factor 1 is a master regulator of breast cancer metastatic niche formation
  publication-title: Proc. Natl Acad. Sci. USA
  doi: 10.1073/pnas.1113483108
  contributor:
    fullname: Wong
– volume: 22
  start-page: 3105
  year: 2016
  end-page: 3117
  ident: CR23
  article-title: NDUFA4L2 fine-tunes oxidative stress in hepatocellular carcinoma
  publication-title: Clin. Cancer Res.
  doi: 10.1158/1078-0432.CCR-15-1987
  contributor:
    fullname: Lai
– volume: 28
  start-page: 511
  year: 2010
  end-page: 515
  ident: CR25
  article-title: Transcript assembly and quantification by RNA-Seq reveals unannotated transcripts and isoform switching during cell differentiation
  publication-title: Nat. Biotechnol.
  doi: 10.1038/nbt.1621
  contributor:
    fullname: Trapnell
– volume: 7
  start-page: 678
  year: 2006
  end-page: 689
  ident: CR18
  article-title: Notch signalling: a simple pathway becomes complex
  publication-title: Nat. Rev. Mol. Cell Biol.
  doi: 10.1038/nrm2009
  contributor:
    fullname: Bray
– volume: 45
  start-page: 279
  year: 2013
  end-page: 284
  ident: CR49
  article-title: The genetic landscape of high-risk neuroblastoma
  publication-title: Nat. Genet
  doi: 10.1038/ng.2529
  contributor:
    fullname: Pugh
– volume: 33
  start-page: 627
  year: 2009
  end-page: 638
  ident: CR39
  article-title: PINK1-associated Parkinson’s disease is caused by neuronal vulnerability to calcium-induced cell death
  publication-title: Mol. Cell
  doi: 10.1016/j.molcel.2009.02.013
  contributor:
    fullname: Gandhi
– volume: 129
  start-page: 111
  year: 2007
  end-page: 122
  ident: CR15
  article-title: HIF-1 regulates cytochrome oxidase subunits to optimize efficiency of respiration in hypoxic cells
  publication-title: Cell
  doi: 10.1016/j.cell.2007.01.047
  contributor:
    fullname: Fukuda
– volume: 213
  start-page: 163
  year: 2016
  end-page: 171
  ident: CR41
  article-title: PINK1 disables the anti-fission machinery to segregate damaged mitochondria for mitophagy
  publication-title: J. Cell Biol.
  doi: 10.1083/jcb.201509003
  contributor:
    fullname: Schapira
– volume: 76
  start-page: 4708
  year: 2016
  end-page: 4719
  ident: CR48
  article-title: PINK1 is a negative regulator of growth and the Warburg effect in glioblastoma
  publication-title: Cancer Res.
  doi: 10.1158/0008-5472.CAN-15-3079
  contributor:
    fullname: Agnihotri
– volume: 389
  start-page: 2492
  issue: 10088
  year: 2017
  end-page: 2502
  ident: CR4
  article-title: Nivolumab in patients with advanced hepatocellular carcinoma (CheckMate 040): an open-label, non-comparative, phase 1/2 dose escalation and expansion trial
  publication-title: The Lancet
  doi: 10.1016/S0140-6736(17)31046-2
  contributor:
    fullname: Melero
– volume: 5
  year: 2014
  ident: CR45
  article-title: PINK1 deficiency sustains cell proliferation by reprogramming glucose metabolism through HIF1
  publication-title: Nat. Commun.
  doi: 10.1038/ncomms5514
  contributor:
    fullname: Requejo-Aguilar
– volume: 9
  start-page: 425
  year: 2006
  end-page: 434
  ident: CR13
  article-title: Attenuation of LDH-A expression uncovers a link between glycolysis, mitochondrial physiology, and tumor maintenance
  publication-title: Cancer Cell
  doi: 10.1016/j.ccr.2006.04.023
  contributor:
    fullname: Leder
– volume: 24
  start-page: 1297
  year: 2015
  end-page: 1308
  ident: CR31
  article-title: Novel basic helix-loop-helix transcription factor hes4 antagonizes the function of twist-1 to regulate lineage commitment of bone marrow stromal/stem cells
  publication-title: Stem Cells Dev.
  doi: 10.1089/scd.2014.0471
  contributor:
    fullname: Cakouros
– volume: 16
  start-page: 157
  year: 2014
  end-page: 166
  ident: CR46
  article-title: Enhancing nucleotide metabolism protects against mitochondrial dysfunction and neurodegeneration in a PINK1 model of Parkinson’s disease
  publication-title: Nat. Cell Biol.
  doi: 10.1038/ncb2901
  contributor:
    fullname: Tufi
– volume: 15
  start-page: 1175
  year: 2016
  end-page: 1189
  ident: CR19
  article-title: Cancer-associated fibroblasts regulate tumor-initiating cell plasticity in hepatocellular carcinoma through c-Met/FRA1/HEY1 signaling
  publication-title: Cell Rep.
  doi: 10.1016/j.celrep.2016.04.019
  contributor:
    fullname: Lau
– volume: 127
  start-page: 1856
  year: 2017
  end-page: 1872
  ident: CR28
  article-title: Folate cycle enzyme MTHFD1L confers metabolic advantages in hepatocellular carcinoma
  publication-title: J. Clin. Invest.
  doi: 10.1172/JCI90253
  contributor:
    fullname: Lee
– volume: 36
  start-page: 1170
  year: 2015
  end-page: 1176
  ident: CR33
  article-title: PI3K isoform-selective inhibitors: next-generation targeted cancer therapies
  publication-title: Acta Pharm. Sin.
  doi: 10.1038/aps.2015.71
  contributor:
    fullname: Meng
– volume: 269
  start-page: 23757
  year: 1994
  end-page: 23763
  ident: CR11
  article-title: Transcriptional regulation of genes encoding glycolytic enzymes by hypoxia-inducible factor 1
  publication-title: J. Biol. Chem.
  doi: 10.1016/S0021-9258(17)31580-6
  contributor:
    fullname: Wang
– volume: 10
  start-page: 25
  year: 2009
  end-page: 34
  ident: CR1
  article-title: Efficacy and safety of sorafenib in patients in the Asia-Pacific region with advanced hepatocellular carcinoma: a phase III randomised, double-blind, placebo-controlled trial
  publication-title: Lancet Oncol.
  doi: 10.1016/S1470-2045(08)70285-7
  contributor:
    fullname: Cheng
– volume: 344
  start-page: 203
  year: 2014
  end-page: 207
  ident: CR36
  article-title: PINK1 loss-of-function mutations affect mitochondrial complex I activity via NdufA10 ubiquinone uncoupling
  publication-title: Science
  doi: 10.1126/science.1249161
  contributor:
    fullname: Morais
– volume: 271
  start-page: 32529
  year: 1996
  end-page: 32537
  ident: CR14
  article-title: Hypoxia response elements in the aldolase A, enolase 1, and lactate dehydrogenase A gene promoters contain essential binding sites for hypoxia-inducible factor 1
  publication-title: J. Biol. Chem.
  doi: 10.1074/jbc.271.51.32529
  contributor:
    fullname: Semenza
– volume: 20
  start-page: 920
  year: 2013
  end-page: 930
  ident: CR37
  article-title: PINK1 protects against cell death induced by mitochondrial depolarization, by phosphorylating Bcl-xL and impairing its pro-apoptotic cleavage
  publication-title: Cell Death Differ.
  doi: 10.1038/cdd.2013.19
  contributor:
    fullname: Arena
– volume: 107
  start-page: 43
  year: 2001
  end-page: 54
  ident: CR7
  article-title: C. elegans EGL-9 and mammalian homologs define a family of dioxygenases that regulate HIF by prolyl hydroxylation
  publication-title: Cell
  doi: 10.1016/S0092-8674(01)00507-4
  contributor:
    fullname: Epstein
– volume: 91
  start-page: 1161
  year: 2011
  end-page: 1218
  ident: CR34
  article-title: What genetics tells us about the causes and mechanisms of Parkinson’s disease
  publication-title: Physiol. Rev.
  doi: 10.1152/physrev.00022.2010
  contributor:
    fullname: Brice
– volume: 290
  start-page: 2798
  year: 2015
  end-page: 2811
  ident: CR40
  article-title: PINK1 kinase catalytic activity is regulated by phosphorylation on serines 228 and 402
  publication-title: J. Biol. Chem.
  doi: 10.1074/jbc.M114.620906
  contributor:
    fullname: Morais
– ident: CR3
– volume: 517
  start-page: 583
  year: 2015
  end-page: 588
  ident: CR24
  article-title: Genome-scale transcriptional activation by an engineered CRISPR-Cas9 complex
  publication-title: Nature
  doi: 10.1038/nature14136
  contributor:
    fullname: Konermann
– volume: 283
  start-page: 10892
  year: 2008
  end-page: 10903
  ident: CR44
  article-title: Mitochondrial autophagy is an HIF-1-dependent adaptive metabolic response to hypoxia
  publication-title: J. Biol. Chem.
  doi: 10.1074/jbc.M800102200
  contributor:
    fullname: Zhang
– volume: 148
  start-page: 399
  year: 2012
  end-page: 408
  ident: CR6
  article-title: Hypoxia-inducible factors in physiology and medicine
  publication-title: Cell
  doi: 10.1016/j.cell.2012.01.021
  contributor:
    fullname: Semenza
– volume: 11
  start-page: 407
  year: 2007
  end-page: 420
  ident: CR17
  article-title: HIF-1 inhibits mitochondrial biogenesis and cellular respiration in VHL-deficient renal cell carcinoma by repression of C-MYC activity
  publication-title: Cancer Cell
  doi: 10.1016/j.ccr.2007.04.001
  contributor:
    fullname: Zhang
– volume: 106
  start-page: 5153
  year: 2009
  end-page: 5158
  ident: CR50
  article-title: FOXO3a-dependent regulation of Pink1 (Park6) mediates survival signaling in response to cytokine deprivation
  publication-title: Proc. Natl Acad. Sci. USA
  doi: 10.1073/pnas.0901104106
  contributor:
    fullname: Mei
– volume: 113
  start-page: E725
  year: 2016
  end-page: E734
  ident: CR30
  article-title: Transketolase counteracts oxidative stress to drive cancer development
  publication-title: Proc. Natl Acad. Sci. USA
  doi: 10.1073/pnas.1508779113
  contributor:
    fullname: Xu
– volume: 68
  start-page: 2551
  year: 2008
  end-page: 2556
  ident: CR47
  article-title: The quest for the 1p36 tumor suppressor
  publication-title: Cancer Res.
  doi: 10.1158/0008-5472.CAN-07-2095
  contributor:
    fullname: Mills
– volume: 9
  start-page: 617
  year: 2005
  end-page: 628
  ident: CR20
  article-title: Hypoxia requires notch signaling to maintain the undifferentiated cell state
  publication-title: Dev. Cell
  doi: 10.1016/j.devcel.2005.09.010
  contributor:
    fullname: Gustafsson
– volume: 9
  start-page: 1243
  year: 2007
  end-page: 1252
  ident: CR38
  article-title: The mitochondrial protease HtrA2 is regulated by Parkinson’s disease-associated kinase PINK1
  publication-title: Nat. Cell Biol.
  doi: 10.1038/ncb1644
  contributor:
    fullname: Plun-Favreau
– volume: 76
  start-page: 2443
  year: 1995
  end-page: 2448
  ident: CR26
  article-title: Prognostic significance of pathologic features of hepatocellular carcinoma. A multivariate analysis of 278 patients
  publication-title: Cancer
  doi: 10.1002/1097-0142(19951215)76:12<2443::AID-CNCR2820761207>3.0.CO;2-F
  contributor:
    fullname: So
– volume: 14
  start-page: 768
  year: 2011
  end-page: 779
  ident: CR16
  article-title: Induction of the mitochondrial NDUFA4L2 protein by HIF-1alpha decreases oxygen consumption by inhibiting Complex I activity
  publication-title: Cell Metab.
  doi: 10.1016/j.cmet.2011.10.008
  contributor:
    fullname: Tello
– volume: 8
  year: 2012
  ident: CR27
  article-title: Target gene analysis by microarrays and chromatin immunoprecipitation identifies HEY proteins as highly redundant bHLH repressors
  publication-title: PLoS Genet.
  doi: 10.1371/journal.pgen.1002728
  contributor:
    fullname: Heisig
– volume: 27
  start-page: 7381
  year: 2007
  end-page: 7393
  ident: CR10
  article-title: Hypoxia-inducible factor 1 and dysregulated c-Myc cooperatively induce vascular endothelial growth factor and metabolic switches hexokinase 2 and pyruvate dehydrogenase kinase 1
  publication-title: Mol. Cell Biol.
  doi: 10.1128/MCB.00440-07
  contributor:
    fullname: Dang
– volume: 9
  start-page: 617
  year: 2005
  ident: 2155_CR20
  publication-title: Dev. Cell
  doi: 10.1016/j.devcel.2005.09.010
  contributor:
    fullname: Gustafsson
– volume: 269
  start-page: 23757
  year: 1994
  ident: 2155_CR11
  publication-title: J. Biol. Chem.
  doi: 10.1016/S0021-9258(17)31580-6
  contributor:
    fullname: GL Semenza
– ident: 2155_CR3
– volume: 20
  start-page: 920
  year: 2013
  ident: 2155_CR37
  publication-title: Cell Death Differ.
  doi: 10.1038/cdd.2013.19
  contributor:
    fullname: G Arena
– volume: 20
  start-page: 4457
  year: 2001
  ident: 2155_CR51
  publication-title: Oncogene
  doi: 10.1038/sj.onc.1204608
  contributor:
    fullname: M Unoki
– volume: 9
  start-page: 425
  year: 2006
  ident: 2155_CR13
  publication-title: Cancer Cell
  doi: 10.1016/j.ccr.2006.04.023
  contributor:
    fullname: VR Fantin
– volume: 91
  start-page: 1161
  year: 2011
  ident: 2155_CR34
  publication-title: Physiol. Rev.
  doi: 10.1152/physrev.00022.2010
  contributor:
    fullname: O Corti
– volume: 76
  start-page: 4708
  year: 2016
  ident: 2155_CR48
  publication-title: Cancer Res.
  doi: 10.1158/0008-5472.CAN-15-3079
  contributor:
    fullname: S Agnihotri
– volume: 9
  start-page: 1243
  year: 2007
  ident: 2155_CR38
  publication-title: Nat. Cell Biol.
  doi: 10.1038/ncb1644
  contributor:
    fullname: H Plun-Favreau
– volume: 106
  start-page: 5153
  year: 2009
  ident: 2155_CR50
  publication-title: Proc. Natl Acad. Sci. USA
  doi: 10.1073/pnas.0901104106
  contributor:
    fullname: Y Mei
– volume: 108
  start-page: 16369
  year: 2011
  ident: 2155_CR22
  publication-title: Proc. Natl Acad. Sci. USA
  doi: 10.1073/pnas.1113483108
  contributor:
    fullname: CC Wong
– volume: 45
  start-page: 279
  year: 2013
  ident: 2155_CR49
  publication-title: Nat. Genet
  doi: 10.1038/ng.2529
  contributor:
    fullname: TJ Pugh
– volume: 344
  start-page: 203
  year: 2014
  ident: 2155_CR36
  publication-title: Science
  doi: 10.1126/science.1249161
  contributor:
    fullname: VA Morais
– volume: 15
  start-page: 1175
  year: 2016
  ident: 2155_CR19
  publication-title: Cell Rep.
  doi: 10.1016/j.celrep.2016.04.019
  contributor:
    fullname: EY Lau
– volume: 4
  year: 2014
  ident: 2155_CR42
  publication-title: Sci. Rep.
  doi: 10.1038/srep06962
  contributor:
    fullname: PI Tsai
– volume: 22
  start-page: 3105
  year: 2016
  ident: 2155_CR23
  publication-title: Clin. Cancer Res.
  doi: 10.1158/1078-0432.CCR-15-1987
  contributor:
    fullname: RK Lai
– volume: 6
  year: 2016
  ident: 2155_CR21
  publication-title: Sci. Rep.
  doi: 10.1038/srep27411
  contributor:
    fullname: Z Qiu
– volume: 27
  start-page: 7381
  year: 2007
  ident: 2155_CR10
  publication-title: Mol. Cell Biol.
  doi: 10.1128/MCB.00440-07
  contributor:
    fullname: JW Kim
– volume: 36
  start-page: 1170
  year: 2015
  ident: 2155_CR33
  publication-title: Acta Pharm. Sin.
  doi: 10.1038/aps.2015.71
  contributor:
    fullname: X Wang
– volume: 8
  start-page: 33
  issue: 1
  year: 2013
  ident: 2155_CR5
  publication-title: Frontiers of Medicine
  doi: 10.1007/s11684-013-0301-3
  contributor:
    fullname: Carmen Chak-Lui Wong
– volume: 33
  start-page: 627
  year: 2009
  ident: 2155_CR39
  publication-title: Mol. Cell
  doi: 10.1016/j.molcel.2009.02.013
  contributor:
    fullname: S Gandhi
– volume: 129
  start-page: 111
  year: 2007
  ident: 2155_CR15
  publication-title: Cell
  doi: 10.1016/j.cell.2007.01.047
  contributor:
    fullname: R Fukuda
– volume: 283
  start-page: 10892
  year: 2008
  ident: 2155_CR44
  publication-title: J. Biol. Chem.
  doi: 10.1074/jbc.M800102200
  contributor:
    fullname: H Zhang
– volume: 14
  start-page: 768
  year: 2011
  ident: 2155_CR16
  publication-title: Cell Metab.
  doi: 10.1016/j.cmet.2011.10.008
  contributor:
    fullname: D Tello
– volume: 5
  year: 2014
  ident: 2155_CR45
  publication-title: Nat. Commun.
  doi: 10.1038/ncomms5514
  contributor:
    fullname: R Requejo-Aguilar
– volume: 76
  start-page: 2443
  year: 1995
  ident: 2155_CR26
  publication-title: Cancer
  doi: 10.1002/1097-0142(19951215)76:12<2443::AID-CNCR2820761207>3.0.CO;2-F
  contributor:
    fullname: IO Ng
– volume: 107
  start-page: 5018
  year: 2010
  ident: 2155_CR43
  publication-title: Proc. Natl Acad. Sci. USA
  doi: 10.1073/pnas.0913485107
  contributor:
    fullname: E Ziviani
– volume: 28
  start-page: 511
  year: 2010
  ident: 2155_CR25
  publication-title: Nat. Biotechnol.
  doi: 10.1038/nbt.1621
  contributor:
    fullname: C Trapnell
– volume: 11
  start-page: 407
  year: 2007
  ident: 2155_CR17
  publication-title: Cancer Cell
  doi: 10.1016/j.ccr.2007.04.001
  contributor:
    fullname: H Zhang
– volume: 16
  start-page: 157
  year: 2014
  ident: 2155_CR46
  publication-title: Nat. Cell Biol.
  doi: 10.1038/ncb2901
  contributor:
    fullname: R Tufi
– volume: 271
  start-page: 32529
  year: 1996
  ident: 2155_CR14
  publication-title: J. Biol. Chem.
  doi: 10.1074/jbc.271.51.32529
  contributor:
    fullname: GL Semenza
– volume: 8
  year: 2012
  ident: 2155_CR27
  publication-title: PLoS Genet.
  doi: 10.1371/journal.pgen.1002728
  contributor:
    fullname: J Heisig
– volume: 517
  start-page: 583
  year: 2015
  ident: 2155_CR24
  publication-title: Nature
  doi: 10.1038/nature14136
  contributor:
    fullname: S Konermann
– volume: 29
  start-page: 565
  year: 2008
  ident: 2155_CR35
  publication-title: Hum. Mutat.
  doi: 10.1002/humu.20719
  contributor:
    fullname: R Marongiu
– volume: 16
  start-page: 702
  year: 2016
  ident: 2155_CR32
  publication-title: Nat. Rev. Immunol.
  doi: 10.1038/nri.2016.93
  contributor:
    fullname: CL Lucas
– volume: 359
  start-page: 378
  year: 2008
  ident: 2155_CR2
  publication-title: N. Engl. J. Med.
  doi: 10.1056/NEJMoa0708857
  contributor:
    fullname: JM Llovet
– volume: 12
  start-page: 149
  year: 1998
  ident: 2155_CR9
  publication-title: Genes Dev.
  doi: 10.1101/gad.12.2.149
  contributor:
    fullname: NV Iyer
– volume: 107
  start-page: 43
  year: 2001
  ident: 2155_CR7
  publication-title: Cell
  doi: 10.1016/S0092-8674(01)00507-4
  contributor:
    fullname: AC Epstein
– volume: 3
  start-page: 177
  year: 2006
  ident: 2155_CR12
  publication-title: Cell Metab.
  doi: 10.1016/j.cmet.2006.02.002
  contributor:
    fullname: JW Kim
– volume: 127
  start-page: 1856
  year: 2017
  ident: 2155_CR28
  publication-title: J. Clin. Invest.
  doi: 10.1172/JCI90253
  contributor:
    fullname: D Lee
– volume: 10
  start-page: 25
  year: 2009
  ident: 2155_CR1
  publication-title: Lancet Oncol.
  doi: 10.1016/S1470-2045(08)70285-7
  contributor:
    fullname: AL Cheng
– volume: 24
  start-page: 1297
  year: 2015
  ident: 2155_CR31
  publication-title: Stem Cells Dev.
  doi: 10.1089/scd.2014.0471
  contributor:
    fullname: D Cakouros
– volume: 92
  start-page: 5510
  year: 1995
  ident: 2155_CR8
  publication-title: Proc. Natl Acad. Sci. USA
  doi: 10.1073/pnas.92.12.5510
  contributor:
    fullname: GL Wang
– volume: 290
  start-page: 2798
  year: 2015
  ident: 2155_CR40
  publication-title: J. Biol. Chem.
  doi: 10.1074/jbc.M114.620906
  contributor:
    fullname: L Aerts
– volume: 68
  start-page: 2551
  year: 2008
  ident: 2155_CR47
  publication-title: Cancer Res.
  doi: 10.1158/0008-5472.CAN-07-2095
  contributor:
    fullname: A Bagchi
– volume: 113
  start-page: E725
  year: 2016
  ident: 2155_CR30
  publication-title: Proc. Natl Acad. Sci. USA
  doi: 10.1073/pnas.1508779113
  contributor:
    fullname: IM Xu
– volume: 389
  start-page: 2492
  issue: 10088
  year: 2017
  ident: 2155_CR4
  publication-title: The Lancet
  doi: 10.1016/S0140-6736(17)31046-2
  contributor:
    fullname: Anthony B El-Khoueiry
– volume: 213
  start-page: 163
  year: 2016
  ident: 2155_CR41
  publication-title: J. Cell Biol.
  doi: 10.1083/jcb.201509003
  contributor:
    fullname: KR Pryde
– volume: 69
  start-page: 1768
  year: 2019
  ident: 2155_CR29
  publication-title: Hepatology
  doi: 10.1002/hep.30467
  contributor:
    fullname: D Lee
– volume: 7
  start-page: 678
  year: 2006
  ident: 2155_CR18
  publication-title: Nat. Rev. Mol. Cell Biol.
  doi: 10.1038/nrm2009
  contributor:
    fullname: SJ Bray
– volume: 148
  start-page: 399
  year: 2012
  ident: 2155_CR6
  publication-title: Cell
  doi: 10.1016/j.cell.2012.01.021
  contributor:
    fullname: GL Semenza
SSID ssj0000330256
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Snippet Hypoxia is commonly found in cancers. Hypoxia, due to the lack of oxygen (O 2 ) as the electron recipient, causes inefficient electron transfer through the...
Hypoxia is commonly found in cancers. Hypoxia, due to the lack of oxygen (O ) as the electron recipient, causes inefficient electron transfer through the...
Abstract Hypoxia is commonly found in cancers. Hypoxia, due to the lack of oxygen (O 2 ) as the electron recipient, causes inefficient electron transfer...
Hypoxia is commonly found in cancers. Hypoxia, due to the lack of oxygen (O2) as the electron recipient, causes inefficient electron transfer through the...
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SubjectTerms 13
13/1
13/106
13/109
13/31
13/51
14
14/28
38
631/67/2327
631/80/86/2366
Animals
Antibodies
Basic Helix-Loop-Helix Transcription Factors - genetics
Basic Helix-Loop-Helix Transcription Factors - metabolism
Biochemistry
Biomedical and Life Sciences
Biosynthesis
Carcinoma, Hepatocellular - metabolism
Carcinoma, Hepatocellular - pathology
Cell Biology
Cell Culture
Cell Cycle Proteins - genetics
Cell Cycle Proteins - metabolism
Cell Hypoxia - genetics
Chromatin
Cristae
Electron transfer
Electron transport chain
Gene expression
HeLa Cells
Hep G2 Cells
Hepatocellular carcinoma
Heterografts
Humans
Hypoxia
Hypoxia-inducible factor 1
Hypoxia-Inducible Factor 1, alpha Subunit - genetics
Hypoxia-Inducible Factor 1, alpha Subunit - metabolism
Hypoxia-inducible factors
Immunology
Immunoprecipitation
Life Sciences
Liver cancer
Liver Neoplasms - metabolism
Liver Neoplasms - pathology
Male
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Nude
Mitochondria
Mitochondria - metabolism
Molecular modelling
Oxidative stress
Protein Kinases - genetics
Protein Kinases - metabolism
PTEN-induced putative kinase
Reactive oxygen species
Regulatory sequences
Therapeutic applications
Transcription
Transcriptomes
Transfection
Tumor Burden - genetics
Tumors
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Title Hypoxia regulates the mitochondrial activity of hepatocellular carcinoma cells through HIF/HEY1/PINK1 pathway
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