ArticleJournal of gastrointestinal oncology2026
Article in Journal of gastrointestinal oncology, 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
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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.
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0 citing papers in PubMed.
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Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related deaths worldwide, with a poor prognosis and high mortality rates. Therapeutic resistance, high recurrence, and limited treatment options contribute to its aggressive nature. The TMF1-regulated nuclear protein 1 (TRNP1) is a highly conserved nuclear protein, recently implicated in tumorigenesis. TRNP1 is upregulated in HCC, but its role in tumorigenesis and immunotherapy resistance remains underexplored. This study investigates the mechanistic roles of TRNP1 in HCC progression through the c-Kit/signal transducers and activators of transcription 3 (STAT3) signaling pathway and its impact on immunotherapy efficacy, particularly in the context of programmed cell death protein 1 (PD-1) blockade. Methods: The expression of TRNP1 was analyzed using bioinformatics tools and confirmed through HCC patient tissue samples. Knockdown and overexpression models of TRNP1 were established in HCC cell lines to investigate its effects on cellular behaviors, including proliferation, migration, invasion, and apoptosis. Transcriptomics explored downstream pathways, identifying the c-Kit/STAT3 signaling axis. Results: TRNP1 was significantly upregulated in HCC tissues compared to adjacent non-cancerous tissues. High TRNP1 expression correlated with reduced overall survival (OS) and disease-free survival (DFS). Conclusions: This study establishes TRNP1 as a tumor-promoting factor in HCC, driving cancer progression via the c-Kit/STAT3 pathway. Moreover,
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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.