ReviewiScience2026
C5aR1 and cGAS/STING and their possible involvement in radiosensitivity of colorectal cancer.
Review in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Worldwide, colorectal cancer (CRC) stands as the third leading cancer in terms of both diagnosis and mortality, underscoring its significant global health impact. Enhancing radiotherapy with radiosensitizers, such as C5aR1 (complement C5a receptor 1) blockade, has shown promise in treating resistant CRC, particularly in immunologically cold tumors. However, the molecular mechanisms by which C5aR1 inhibition improves radiosensitivity remain to be clarified. Reduced cGAS/STING (cyclic guanosine monophosphate-adenosine monophosphate synthase/stimulator of interferon genes) pathway activity is linked to radioresistance, while radiotherapy-induced cGAS/STING activation increases IFNB1 (interferon beta 1) and impairs DNA repair. Conversely, the complement component 5a (C5a)/C5aR1 axis suppresses STING-driven IFNB1 expression in immune responses, suggesting their distinct regulatory effects on cancer cell radiotherapy responses. Targeting C5aR1 may therefore enhance radiosensitivity by modulating the cGAS/STING pathway. This review examines potential interactions between C5aR1 and the cGAS/STING pathway, highlighting their relevance to addressing resistance mechanisms in CRC.
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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 Socratic graph.