Hypoxia inducible factor HIF-1 promotes myeloid-derived suppressor cells accumulation through ENTPD2/CD39L1 in hepatocellular carcinoma

Myeloid-derived suppressor cells (MDSCs) possess immunosuppressive activities, which allow cancers to escape immune surveillance and become non-responsive to immune checkpoints blockade. Here we report hypoxia as a cause of MDSC accumulation. Using hepatocellular carcinoma (HCC) as a cancer model, w...

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Published inNature communications Vol. 8; no. 1; pp. 517 - 12
Main Authors Chiu, David Kung-Chun, Tse, Aki Pui-Wah, Xu, Iris Ming-Jing, Di Cui, Jane, Lai, Robin Kit-Ho, Li, Lynna Lan, Koh, Hui-Yu, Tsang, Felice Ho-Ching, Wei, Larry Lai, Wong, Chun-Ming, Ng, Irene Oi-Lin, Wong, Carmen Chak-Lui
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 11.09.2017
Nature Publishing Group
Nature Portfolio
Subjects
631/67/1504/1610/4029
631/67/327
631/67/580
AMP
Cancer
Differentiation
Hepatocellular carcinoma
Humanities and Social Sciences
Hypoxia
Hypoxia-inducible factor 1
Hypoxia-inducible factors
Immune checkpoint
Immune checkpoint inhibitors
Immunosuppression
Immunosurveillance
Liver cancer
multidisciplinary
Science
Science (multidisciplinary)
Suppressor cells
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Abstract Myeloid-derived suppressor cells (MDSCs) possess immunosuppressive activities, which allow cancers to escape immune surveillance and become non-responsive to immune checkpoints blockade. Here we report hypoxia as a cause of MDSC accumulation. Using hepatocellular carcinoma (HCC) as a cancer model, we show that hypoxia, through stabilization of hypoxia-inducible factor-1 (HIF-1), induces ectoenzyme, ectonucleoside triphosphate diphosphohydrolase 2 (ENTPD2/CD39L1), in cancer cells, causing its overexpression in HCC clinical specimens. Overexpression of ENTPD2 is found as a poor prognostic indicator for HCC. Mechanistically, we demonstrate that ENTPD2 converts extracellular ATP to 5′-AMP, which prevents the differentiation of MDSCs and therefore promotes the maintenance of MDSCs. We further find that ENTPD2 inhibition is able to mitigate cancer growth and enhance the efficiency and efficacy of immune checkpoint inhibitors. Our data suggest that ENTPD2 may be a good prognostic marker and therapeutic target for cancer patients, especially those receiving immune therapy. Myeloid-derived suppressor cells (MDSCs) promote tumor immune escape. Here, the authors show that in hepatocellular carcinoma, hypoxia induces the expression of ENTPD2 on cancer cells leading to elevated extracellular 5′-AMP, which in turn promote the maintenance of MDSCs by preventing their differentiation.
AbstractList Myeloid-derived suppressor cells (MDSCs) possess immunosuppressive activities, which allow cancers to escape immune surveillance and become non-responsive to immune checkpoints blockade. Here we report hypoxia as a cause of MDSC accumulation. Using hepatocellular carcinoma (HCC) as a cancer model, we show that hypoxia, through stabilization of hypoxia-inducible factor-1 (HIF-1), induces ectoenzyme, ectonucleoside triphosphate diphosphohydrolase 2 (ENTPD2/CD39L1), in cancer cells, causing its overexpression in HCC clinical specimens. Overexpression of ENTPD2 is found as a poor prognostic indicator for HCC. Mechanistically, we demonstrate that ENTPD2 converts extracellular ATP to 5′-AMP, which prevents the differentiation of MDSCs and therefore promotes the maintenance of MDSCs. We further find that ENTPD2 inhibition is able to mitigate cancer growth and enhance the efficiency and efficacy of immune checkpoint inhibitors. Our data suggest that ENTPD2 may be a good prognostic marker and therapeutic target for cancer patients, especially those receiving immune therapy.
Myeloid-derived suppressor cells (MDSCs) promote tumor immune escape. Here, the authors show that in hepatocellular carcinoma, hypoxia induces the expression of ENTPD2 on cancer cells leading to elevated extracellular 5′-AMP, which in turn promote the maintenance of MDSCs by preventing their differentiation.
Myeloid-derived suppressor cells (MDSCs) possess immunosuppressive activities, which allow cancers to escape immune surveillance and become non-responsive to immune checkpoints blockade. Here we report hypoxia as a cause of MDSC accumulation. Using hepatocellular carcinoma (HCC) as a cancer model, we show that hypoxia, through stabilization of hypoxia-inducible factor-1 (HIF-1), induces ectoenzyme, ectonucleoside triphosphate diphosphohydrolase 2 (ENTPD2/CD39L1), in cancer cells, causing its overexpression in HCC clinical specimens. Overexpression of ENTPD2 is found as a poor prognostic indicator for HCC. Mechanistically, we demonstrate that ENTPD2 converts extracellular ATP to 5′-AMP, which prevents the differentiation of MDSCs and therefore promotes the maintenance of MDSCs. We further find that ENTPD2 inhibition is able to mitigate cancer growth and enhance the efficiency and efficacy of immune checkpoint inhibitors. Our data suggest that ENTPD2 may be a good prognostic marker and therapeutic target for cancer patients, especially those receiving immune therapy. Myeloid-derived suppressor cells (MDSCs) promote tumor immune escape. Here, the authors show that in hepatocellular carcinoma, hypoxia induces the expression of ENTPD2 on cancer cells leading to elevated extracellular 5′-AMP, which in turn promote the maintenance of MDSCs by preventing their differentiation.
Myeloid-derived suppressor cells (MDSCs) possess immunosuppressive activities, which allow cancers to escape immune surveillance and become non-responsive to immune checkpoints blockade. Here we report hypoxia as a cause of MDSC accumulation. Using hepatocellular carcinoma (HCC) as a cancer model, we show that hypoxia, through stabilization of hypoxia-inducible factor-1 (HIF-1), induces ectoenzyme, ectonucleoside triphosphate diphosphohydrolase 2 (ENTPD2/CD39L1), in cancer cells, causing its overexpression in HCC clinical specimens. Overexpression of ENTPD2 is found as a poor prognostic indicator for HCC. Mechanistically, we demonstrate that ENTPD2 converts extracellular ATP to 5'-AMP, which prevents the differentiation of MDSCs and therefore promotes the maintenance of MDSCs. We further find that ENTPD2 inhibition is able to mitigate cancer growth and enhance the efficiency and efficacy of immune checkpoint inhibitors. Our data suggest that ENTPD2 may be a good prognostic marker and therapeutic target for cancer patients, especially those receiving immune therapy.Myeloid-derived suppressor cells (MDSCs) promote tumor immune escape. Here, the authors show that in hepatocellular carcinoma, hypoxia induces the expression of ENTPD2 on cancer cells leading to elevated extracellular 5'-AMP, which in turn promote the maintenance of MDSCs by preventing their differentiation.
Myeloid-derived suppressor cells (MDSCs) possess immunosuppressive activities, which allow cancers to escape immune surveillance and become non-responsive to immune checkpoints blockade. Here we report hypoxia as a cause of MDSC accumulation. Using hepatocellular carcinoma (HCC) as a cancer model, we show that hypoxia, through stabilization of hypoxia-inducible factor-1 (HIF-1), induces ectoenzyme, ectonucleoside triphosphate diphosphohydrolase 2 (ENTPD2/CD39L1), in cancer cells, causing its overexpression in HCC clinical specimens. Overexpression of ENTPD2 is found as a poor prognostic indicator for HCC. Mechanistically, we demonstrate that ENTPD2 converts extracellular ATP to 5'-AMP, which prevents the differentiation of MDSCs and therefore promotes the maintenance of MDSCs. We further find that ENTPD2 inhibition is able to mitigate cancer growth and enhance the efficiency and efficacy of immune checkpoint inhibitors. Our data suggest that ENTPD2 may be a good prognostic marker and therapeutic target for cancer patients, especially those receiving immune therapy.Myeloid-derived suppressor cells (MDSCs) promote tumor immune escape. Here, the authors show that in hepatocellular carcinoma, hypoxia induces the expression of ENTPD2 on cancer cells leading to elevated extracellular 5'-AMP, which in turn promote the maintenance of MDSCs by preventing their differentiation.Myeloid-derived suppressor cells (MDSCs) possess immunosuppressive activities, which allow cancers to escape immune surveillance and become non-responsive to immune checkpoints blockade. Here we report hypoxia as a cause of MDSC accumulation. Using hepatocellular carcinoma (HCC) as a cancer model, we show that hypoxia, through stabilization of hypoxia-inducible factor-1 (HIF-1), induces ectoenzyme, ectonucleoside triphosphate diphosphohydrolase 2 (ENTPD2/CD39L1), in cancer cells, causing its overexpression in HCC clinical specimens. Overexpression of ENTPD2 is found as a poor prognostic indicator for HCC. Mechanistically, we demonstrate that ENTPD2 converts extracellular ATP to 5'-AMP, which prevents the differentiation of MDSCs and therefore promotes the maintenance of MDSCs. We further find that ENTPD2 inhibition is able to mitigate cancer growth and enhance the efficiency and efficacy of immune checkpoint inhibitors. Our data suggest that ENTPD2 may be a good prognostic marker and therapeutic target for cancer patients, especially those receiving immune therapy.Myeloid-derived suppressor cells (MDSCs) promote tumor immune escape. Here, the authors show that in hepatocellular carcinoma, hypoxia induces the expression of ENTPD2 on cancer cells leading to elevated extracellular 5'-AMP, which in turn promote the maintenance of MDSCs by preventing their differentiation.
ArticleNumber 517
Author Xu, Iris Ming-Jing
Wong, Chun-Ming
Tse, Aki Pui-Wah
Tsang, Felice Ho-Ching
Wong, Carmen Chak-Lui
Di Cui, Jane
Li, Lynna Lan
Koh, Hui-Yu
Chiu, David Kung-Chun
Wei, Larry Lai
Ng, Irene Oi-Lin
Lai, Robin Kit-Ho
Author_xml – sequence: 1
  givenname: David Kung-Chun
  surname: Chiu
  fullname: Chiu, David Kung-Chun
  organization: Department of Pathology, The University of Hong Kong
– sequence: 2
  givenname: Aki Pui-Wah
  surname: Tse
  fullname: Tse, Aki Pui-Wah
  organization: Department of Pathology, The University of Hong Kong
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  givenname: Iris Ming-Jing
  surname: Xu
  fullname: Xu, Iris Ming-Jing
  organization: Department of Pathology, The University of Hong Kong
– sequence: 4
  givenname: Jane
  surname: Di Cui
  fullname: Di Cui, Jane
  organization: Department of Pathology, The University of Hong Kong
– sequence: 5
  givenname: Robin Kit-Ho
  surname: Lai
  fullname: Lai, Robin Kit-Ho
  organization: Department of Pathology, The University of Hong Kong
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  surname: Li
  fullname: Li, Lynna Lan
  organization: Department of Pathology, The University of Hong Kong
– sequence: 7
  givenname: Hui-Yu
  surname: Koh
  fullname: Koh, Hui-Yu
  organization: Department of Pathology, The University of Hong Kong
– sequence: 8
  givenname: Felice Ho-Ching
  surname: Tsang
  fullname: Tsang, Felice Ho-Ching
  organization: Department of Pathology, The University of Hong Kong
– sequence: 9
  givenname: Larry Lai
  surname: Wei
  fullname: Wei, Larry Lai
  organization: Department of Pathology, The University of Hong Kong
– sequence: 10
  givenname: Chun-Ming
  orcidid: 0000-0002-2497-7858
  surname: Wong
  fullname: Wong, Chun-Ming
  organization: Department of Pathology, The University of Hong Kong, State Key Laboratory for Liver Research, The University of Hong Kong
– sequence: 11
  givenname: Irene Oi-Lin
  surname: Ng
  fullname: Ng, Irene Oi-Lin
  email: iolng@hku.hk
  organization: Department of Pathology, The University of Hong Kong, State Key Laboratory for Liver Research, The University of Hong Kong
– sequence: 12
  givenname: Carmen Chak-Lui
  surname: Wong
  fullname: Wong, Carmen Chak-Lui
  email: carmencl@pathology.hku.hk
  organization: Department of Pathology, The University of Hong Kong, State Key Laboratory for Liver Research, The University of Hong Kong
BackLink https://www.ncbi.nlm.nih.gov/pubmed/28894087$$D View this record in MEDLINE/PubMed
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Snippet Myeloid-derived suppressor cells (MDSCs) possess immunosuppressive activities, which allow cancers to escape immune surveillance and become non-responsive to...
Myeloid-derived suppressor cells (MDSCs) promote tumor immune escape. Here, the authors show that in hepatocellular carcinoma, hypoxia induces the expression...
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StartPage 517
SubjectTerms 631/67/1504/1610/4029
631/67/327
631/67/580
AMP
Cancer
Differentiation
Hepatocellular carcinoma
Humanities and Social Sciences
Hypoxia
Hypoxia-inducible factor 1
Hypoxia-inducible factors
Immune checkpoint
Immune checkpoint inhibitors
Immunosuppression
Immunosurveillance
Liver cancer
multidisciplinary
Science
Science (multidisciplinary)
Suppressor cells
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Title Hypoxia inducible factor HIF-1 promotes myeloid-derived suppressor cells accumulation through ENTPD2/CD39L1 in hepatocellular carcinoma
URI https://link.springer.com/article/10.1038/s41467-017-00530-7
https://www.ncbi.nlm.nih.gov/pubmed/28894087
https://www.proquest.com/docview/1937697016
https://www.proquest.com/docview/1938200901
https://pubmed.ncbi.nlm.nih.gov/PMC5593860
https://doaj.org/article/360a1c2886224e2282f3c6518e7a0d34
Volume 8
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