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Cited by 101Phagocytosis and Immune RegulationCell death mechanisms and regulationAutophagy in Disease and Therapy

The DOI matches its Crossref record; 146 of the 146 references it cites were found in a registry or an index.

Regulation of efferocytosis as a novel cancer therapy

Open access
Zhou, Yunxiang, Yao, Yihan, Deng, Yongchuan, Shao, Anwen·2020·Cell Communication and Signaling
DOI 10.1186/s12964-020-00542-9PMC PMC7199874
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Abstract

Efferocytosis is a physiologic phagocytic clearance of apoptotic cells, which modulates inflammatory responses and the immune environment and subsequently facilitates immune escape of cancer cells, thus promoting tumor development and progression. Efferocytosis is an equilibrium formed by perfect coordination among “find-me”, “eat-me” and “don’t-eat-me” signals. These signaling pathways not only affect the proliferation, invasion, metastasis, and angiogenesis of tumor cells but also regulate adaptive responses and drug resistance to antitumor therapies. Therefore, efferocytosis-related molecules and pathways are potential targets for antitumor therapy. Besides, supplementing conventional chemotherapy, radiotherapy and other immunotherapies with efferocytosis-targeted therapy could enhance the therapeutic efficacy, reduce off-target toxicity, and promote patient outcome.

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Fig. 1 Schematic representation of signaling pathways in the efferocytosis-induced immune suppression for tumor progression. The engulfment of apoptotic cells by tumor-associated macrophages triggers a series of signaling pathways, subsequently induces M2 polarization of macrophages while inhibiting M1 polarization, increases Treg cells while decreasing CD8+ T cells, and thereby resulting in the inflammation resolution and immune suppression, which may provide an environment for cancer to escape from immunological surveillance and promote tumor progression. NFκB = factor-κ-gene binding; JAK/STAT1 = Janus kinase/signal transducers and activators of transcription 1; PI3K/Akt = phosphatidylinositol 3 kinase/protein-serine-threonine kinase; PD-1/PD-L1 = programmed death-ligand 1/programmed cell death protein 1; TLR = Toll-like receptor; IL = interleukin; TGFβ = transforming growth factor-beta; PGE2 = prostaglandin E2; PAF = platelet-activating factor; TNF-α = tumor necrosis factor-alpha; Treg cells = regulatory t cell
Fig. 1 Schematic representation of signaling pathways in the efferocytosis-induced immune suppression for tumor progression. The engulfment of apoptotic cells by tumor-associated macrophages triggers a series of signaling pathways, subsequently induces M2 polarization of macrophages while inhibiting M1 polarization, increases Treg cells while decreasing CD8+ T cells, and thereby resulting in the inflammation resolution and immune suppression, which may provide an environment for cancer to escape from immunological surveillance and promote tumor progression. NFκB = factor-κ-gene binding; JAK/STAT1 = Janus kinase/signal transducers and activators of transcription 1; PI3K/Akt = phosphatidylinositol 3 kinase/protein-serine-threonine kinase; PD-1/PD-L1 = programmed death-ligand 1/programmed cell death protein 1; TLR = Toll-like receptor; IL = interleukin; TGFβ = transforming growth factor-beta; PGE2 = prostaglandin E2; PAF = platelet-activating factor; TNF-α = tumor necrosis factor-alpha; Treg cells = regulatory t cellCC BY · PubMed Central

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Metadata

Authors
Zhou, Y., Yao, Y., Deng, Y., & Shao, A.
Affiliations
Second Affiliated Hospital of Zhejiang University (CN)
Corresponding author
  • Deng, Yongchuan
  • Shao, Anwen
ORCID
Venue
Cell Communication and Signaling
Publisher
Springer Science and Business Media LLC
Published
2020-05-05
Volume
18
Issue
1
Pages
71-71
ISSN
1478-811X (ISSN-L)
DOI
10.1186/s12964-020-00542-9
PMC
PMC7199874
OpenAlex
W3023079876
Cited by
100
References
146
Citations by year
2026: 8 · 2025: 23 · 2024: 29 · 2023: 17 · 2022: 11 · 2021: 8 · 2020: 4
FWCI
0.98
Type
journal article
Language
en
Open access
Licence
Locations
  • Cell Communication and Signaling (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Postdoctoral Research Foundation of China (2017M612010)
  • National Natural Science Foundation of China (81701144)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
Keywords
efferocytosis, cancer immunotherapy, tumor immune evasion, find-me signals, eat-me signals, don't eat me signal, tumor microenvironment, drug resistance, combination therapy, cancer therapy targets
MeSH terms
Regulated Cell Death, Animals, Humans, Immunosuppression Therapy, Inflammation, Neoplasms, Phagocytosis, Apoptosis, Disease Progression, Tumor Escape

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