ReviewNaunyn-Schmiedeberg's archives of pharmacology2025
Deciphering cGAS-STING signaling: implications for tumor immunity and hepatocellular carcinoma.
Review in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Molecular Mechanisms of cGAS-STING Axis and Mitochondrial Dysfunction-Related Diseases in Humans: A Comprehensive Review.Current neuropharmacology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is the most prevalent form of primary liver cancer and poses a significant global health challenge due to its rising incidence and associated mortality. Recent advancements in understanding the cytosolic DNA sensing, the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway have illuminated its critical role in the immune response to HCC. This narrative review deciphers the multifaceted involvement of cGAS-STING in HCC, mainly its function in detecting cytosolic DNA and initiating type I interferon (IFN-I) responses, which are pivotal for antitumor immunity. This immune response is crucial for combating pathogens and can play a role in tumor surveillance. In the context of HCC, the tumor microenvironment (TME) can exhibit immune resistance, which complicates the effectiveness of therapies like immune checkpoint blockade. However, activation of the cGAS-STING pathway has been shown to stimulate antitumor immune responses, enhancing the activity of dendritic cells and cytotoxic T lymphocytes. There is ongoing research into STING agonists as a treatment strategy for HCC, with some studies indicating promising results in prolonging survival and enhancing the immune response against tumors. By summarizing current knowledge and identifying research gaps, this review aims to provide a comprehensive overview of cGAS-STING signaling in HCC and its future directions, emphasizing its potential as a therapeutic target in the fight against HCC. Understanding these mechanisms could pave the way for innovative immunotherapeutic approaches that enhance the efficacy of existing treatments and improve patient prognosis.
Indexed as
Identifiers
40332552What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.