ArticleDigestive diseases and sciences2025
AIF1 Regulates the Progression of Esophageal Squamous Cell Carcinoma Through Negative Regulation of Immune T Cell Efflux Function by TIGIT Signal.
Article in Digestive diseases and sciences, 2025. 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
backgroundEsophageal cancer stands as one of the most aggressive and lethal malignancies among digestive tract tumors.
aimsThis study aimed to explore whether AIF1 regulated immune infiltration in esophageal cancer and its association with TIGIT.
methodsAKR cells transfected with an AIF1 overexpression vector were subcutaneously injected into mice. Additionally, mice were treated with a TIGIT monoclonal antibody. Tumor growth was monitored, and the proportions of different T cell subsets in tumor tissues were detected. AKR cells transfected with AIF1 and Treg cells transfected with TIGIT were co-cultured. Cell viability was assessed using the CCK-8 assay. The expression levels of immune infiltration-related markers (FOXP3, TIM3, and IL-6) were detected by ELISA or Western blotting.
resultsOverexpression of AIF1 combined with TIGIT mAb treatment inhibited tumor growth. This combination promoted the expression of CD3⁺ and IFN-γ (markers of effector T cells) and suppressed the expression of FOXP3 and TIM3 (markers related to immune suppression). In the AIF/TIGIT-treated group, the expressions of pro-inflammatory cytokines (IFN-γ, IL-6, and TNF-α) were up-regulated, while the expressions of anti-inflammatory cytokines (TNF-β and IL-10) were down-regulated. AIF/TIGIT treatment significantly inhibited the expression of immune-specific factors PD-1, FOXP3 in the tissue cells. When TIGIT-overexpressing T cells were co-cultured with cancer cells, cell viability was lower compared to the group with AIF1 overexpression alone. Notably, the group with both AIF1 overexpression and TIGIT overexpression exhibited the lowest cell viability. Under conditions of AIF1 overexpression and TIGIT overexpression, the levels of LDH, TNF-α, and IFN-γ in cancer cells were also the lowest, indicating a synergistic effect on modulating cell function and cytokine secretion.
conclusionsAIF1 may regulate the progression of esophageal squamous cell carcinoma by negatively modulating the efflux function of immune T cells via the TIGIT signaling pathway.
Indexed as
Identifiers
40830317What 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.