ArticleOncogenesis2026
C1s protects cutaneous squamous carcinoma cells from TRAIL-induced apoptosis.
Article in Oncogenesis, 2026. 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.
- Tumour cell-intrinsic complement C1r and C1s regulate cancer cell fitness and shape the immune microenvironment in triple-negative breast cancer.Cellular and molecular life sciences : CMLS · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Cutaneous squamous cell carcinoma (cSCC) is the most common metastatic skin cancer. The prognosis of the metastatic cSCC is poor, and there are no established biomarkers to predict metastasis risk, nor specific targeted therapies for advanced or metastatic cSCC. Previous studies have demonstrated that the complement serine proteinase C1s promotes cSCC growth both in culture and in vivo by modulating apoptotic signaling. Here, we investigated the mechanistic role of C1s in regulating apoptosis by examining its impact on cell surface proteome of cSCC cells. Mass spectrometric analysis of cell surface proteins following silencing of C1s identified TRAIL receptor 1 (DR4) as a candidate target, showing increased accumulation at the cell surface. This finding was validated using cell surface biotinylation and western blot analysis in both siRNA-mediated C1s knockdown and CRISPR/Cas9-generated C1s knockout cells. Functionally, high endogenous levels or forced overexpression of C1s conferred resistance to TRAIL-induced apoptosis in cSCC cells, whereas reduced C1s levels sensitized cells to apoptotic signaling. These findings suggest that upregulation of complement C1s in cSCC not only contributes to tumor progression but also serves as a protective mechanism against TRAIL-induced apoptosis, highlighting its potential as a therapeutic target and biomarker in aggressive cSCC.
Identifiers
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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 OpenQuestion graph.