ArticleOncoimmunology2025
Smad7 is a negative regulator of immunogenic cell death in colorectal cancer.
Article in Oncoimmunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- SMAD7-Associated Glycolytic Regulation Promotes Lactate-Dependent Macrophage Phenotype Modulation in Colorectal Cancer.Cancers · 2026Article
- Leveraging multimodal cancer immunotherapy to amplify the efficacy of oncolytic viruses.Experimental hematology & oncology · 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Induction of endoplasmic reticulum (ER) stress is followed by exposure of calreticulin (CRT) on the cancer cell plasma membrane and elicits an anticancer immune response, referred to as immunogenic cell death (ICD). Smad7 is highly expressed by colorectal cancer (CRC) cells, and its knockdown with a specific antisense oligonucleotide (AS) induces ER stress. We hypothesized that, by preventing ER stress, high Smad7 in CRC cells can contribute to limiting ICD. This study aimed to investigate whether targeted inhibition of Smad7 in CRC cells promotes an anti-cancer immune response. Downregulation of Smad7 in the human HCT116 and DLD1 cells and murine CT26 cells promoted calreticulin translocation to the plasma membrane and this phenomenon was prevented by Tauro-urso-deoxycholic acid, an inhibitor of ER stress. Smad7-deficient cells secreted high levels of ATP and HMGB1, thereby promoting the activation of co-cultured dendritic cells. Mice engrafted with Smad7-deficient CT26 cells developed fewer and smaller tumors than wild-type CT26 cell-engrafted mice and exhibited a marked tumor infiltration with CD8
Indexed as
Identifiers
What 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.