Emerging roles of class I PI3K inhibitors in modulating tumor microenvironment and immunity

Immune system-mediated tumor killing has revolutionized anti-tumor therapies, providing long-term and durable responses in some patients. The phosphoinositide 3-kinase (PI3K) pathway controls multiple biological processes and is frequently dysregulated in malignancies. Enormous efforts have been mad...

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Published inActa pharmacologica Sinica Vol. 41; no. 11; pp. 1395 - 1402
Main Authors Sun, Pu, Meng, Ling-Hua
Format Journal Article
LanguageEnglish
Published United States Nature Publishing Group 01.11.2020
Springer Singapore
Subjects
1-Phosphatidylinositol 3-kinase
Adapter proteins
Angiogenesis
Bone marrow
Cancer
Cell growth
Cytokines
Cytotoxicity
FDA approval
Growth factors
Immune system
Immunotherapy
Kinases
Lymphocytes
Lymphoma
Metabolism
Motility
Mutation
Review
phosphoinositide 3-kinase (PI3K)
immune cells
tumor microenvironment
PI3K inhibitors
immunotherapy
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Abstract Immune system-mediated tumor killing has revolutionized anti-tumor therapies, providing long-term and durable responses in some patients. The phosphoinositide 3-kinase (PI3K) pathway controls multiple biological processes and is frequently dysregulated in malignancies. Enormous efforts have been made to develop inhibitors against class I PI3K. Notably, with the increasing understanding of PI3K, it has been widely accepted that PI3K inhibition not only restrains tumor progression, but also reshapes the immunosuppressive tumor microenvironment. In this review, we focus on the pivotal roles of class I PI3Ks in adaptive and innate immune cells, as well as other stromal components. We discuss the modulation by PI3K inhibitors of the tumor-supportive microenvironment, including eliminating the regulatory immune cells, restoring cytotoxic cells or regulating angiogenesis. The potential combinations of PI3K inhibitors with other therapies to enhance the anti-tumor immunity are also described.
AbstractList Immune system-mediated tumor killing has revolutionized anti-tumor therapies, providing long-term and durable responses in some patients. The phosphoinositide 3-kinase (PI3K) pathway controls multiple biological processes and is frequently dysregulated in malignancies. Enormous efforts have been made to develop inhibitors against class I PI3K. Notably, with the increasing understanding of PI3K, it has been widely accepted that PI3K inhibition not only restrains tumor progression, but also reshapes the immunosuppressive tumor microenvironment. In this review, we focus on the pivotal roles of class I PI3Ks in adaptive and innate immune cells, as well as other stromal components. We discuss the modulation by PI3K inhibitors of the tumor-supportive microenvironment, including eliminating the regulatory immune cells, restoring cytotoxic cells or regulating angiogenesis. The potential combinations of PI3K inhibitors with other therapies to enhance the anti-tumor immunity are also described.
Author Meng, Ling-Hua
Sun, Pu
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  surname: Sun
  fullname: Sun, Pu
  organization: University of Chinese Academy of Sciences, Beijing, 100049, China
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  fullname: Meng, Ling-Hua
  email: lhmeng@simm.ac.cn, lhmeng@simm.ac.cn
  organization: University of Chinese Academy of Sciences, Beijing, 100049, China. lhmeng@simm.ac.cn
BackLink https://www.ncbi.nlm.nih.gov/pubmed/32939035$$D View this record in MEDLINE/PubMed
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Keywords phosphoinositide 3-kinase (PI3K)
immune cells
tumor microenvironment
PI3K inhibitors
immunotherapy
Language English
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SSID ssj0032319
Score 2.4690948
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Snippet Immune system-mediated tumor killing has revolutionized anti-tumor therapies, providing long-term and durable responses in some patients. The phosphoinositide...
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SubjectTerms 1-Phosphatidylinositol 3-kinase
Adapter proteins
Angiogenesis
Bone marrow
Cancer
Cell growth
Cytokines
Cytotoxicity
FDA approval
Growth factors
Immune system
Immunotherapy
Kinases
Lymphocytes
Lymphoma
Metabolism
Motility
Mutation
Review
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Title Emerging roles of class I PI3K inhibitors in modulating tumor microenvironment and immunity
URI https://www.ncbi.nlm.nih.gov/pubmed/32939035
https://www.proquest.com/docview/2471529310/abstract/
https://search.proquest.com/docview/2443880842
https://pubmed.ncbi.nlm.nih.gov/PMC7656798
Volume 41
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