Role of the cGAS–STING pathway in cancer development and oncotherapeutic approaches
Open accessAbstract
The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway mediates anti-microbial innate immunity by inducing the production of type I interferons (IFNs) and inflammatory cytokines upon recognition of microbial DNA. Recent studies reveal that self-DNA from tumors and by-products of genomic instability also activates the cGAS-STING pathway and either promotes or inhibits tumor development. This has led to the development of cancer therapeutics using STING agonists alone and in combination with conventional cancer treatment or immune checkpoint targeting. On the other hand, for cancers lacking the cGAS-STING pathway and thus a regular innate immunity response, oncolytic virus therapy has been shown to have therapeutic potential. We here review and discuss the dichotomous roles of the cGAS-STING pathway in cancer development and therapeutic approaches.
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Cytosolic chromatin fragments and micronuclei are commonly accumulated during malignant transformation, increasing the probability of cytosolic DNA leakage in cancer cells or tumor-derived DNA uptake in DCs.
“Cytosolic chromatin fragments and micronuclei are commonly accumulated during malignant transformation, increasing the probability of cytosolic DNA leakage in cancer cells or tumor-derived DNA uptake in DCs [256].”
From Combination strategies with PD-1/PD-L1 blockade: current advances and future directions (2022) · cites this paper as [256]
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Extrachromosomal telomere repeat DNA is linked to ALT development via cGAS-STING DNA sensing pathway
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Self-citationDiverse roles of STING-dependent signaling on the development of cancer
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Replication of Telomeres and the Regulation of TelomerasePreprint
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Telomerase-Independent Paths to Immortality in Predictable Cancer Subtypes
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Flagged first, then by citations
Cited by
Sorted by citations
Combination strategies with PD-1/PD-L1 blockade: current advances and future directions
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Activating cGAS-STING pathway for the optimal effect of cancer immunotherapy
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Prospects for combining immune checkpoint blockade with PARP inhibition
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“As a result, these DNA damages persist in a low level which might increase the possibility of the exposure of doublestrand DNA (dsDNA) in cytoplasm [97].”
BackgroundType I interferons and dendritic cells in cancer immunotherapy
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Type I interferons and endoplasmic reticulum stress in health and disease
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cGAS-STING signaling encourages immune cell overcoming of fibroblast barricades in pancreatic cancer
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- Authors
- Khoo, L. T., & Chen, L.
- Affiliations
- Institute of Molecular Biology, Academia Sinica (TW)
- Corresponding author
- Chen, Liuh‐Yow
- Venue
- The EMBO Reports
- Published
- 2018-11-16
- Volume
- 19
- Issue
- 12
- ISSN
- 1469-221X (ISSN-L)
- 1469-3178
- PMC
- PMC6280650
- OpenAlex
- W2900458154
- Cited by
- 204
- References
- 95
- Citations by year
- 2026: 13 · 2025: 30 · 2024: 29 · 2023: 49 · 2022: 26 · 2021: 25 · 2020: 16 · 2019: 16
- FWCI
- 1.46
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- EMBO Reports (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministry of Science and Technology (105‐2311‐B‐001‐055‐MY3)
- Academia Sinica (CDA‐105‐L01)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Keywords
- cGAS-STING pathway, carcinogenesis, STING agonist, type I interferon, genomic instability, innate immunity, cancer therapy, immune checkpoint inhibitors, oncolytic virotherapy, cancer immunotherapy
- MeSH terms
- Animals, Humans, Membrane Proteins, Neoplasms, Nucleotidyltransferases, Signal Transduction, Telomere, Carcinogenesis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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