ArticleMedical oncology (Northwood, London, England)2025
BNC2 as a novel driver of pancreatic cancer progression through transcriptional regulation of COL3A1 and epithelial-to-mesenchymal transition.
Article in Medical oncology (Northwood, London, England), 2025. 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
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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.
Who cites it
1 citing paper in PubMed.
- Peritoneal metastasis in pancreatic cancer: molecular mechanisms, microenvironmental remodeling, and emerging intraperitoneal interventions.Frontiers in molecular biosciences · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Pancreatic cancer remains one of the deadliest malignancies due to its high metastatic potential and resistance to treatment. Transcription factors driving epithelial-to-mesenchymal transition (EMT) are critical in promoting invasion and metastasis, yet their full repertoire remains poorly understood. Here, we identify Basonuclin 2 (BNC2), a zinc-finger transcription factor, as a novel regulator of pancreatic cancer progression. Through integrative transcriptomic analyses, we demonstrate that BNC2 is significantly upregulated in pancreatic cancer and correlates with advanced tumor grade, stage, and poor prognosis. Functional assays reveal that BNC2 promotes EMT and cancer cell invasion by transcriptionally activating collagen type III alpha 1 (COL3A1), a key extracellular matrix component. Knockdown of BNC2 suppresses EMT, reduces invasiveness, and downregulates COL3A1, whereas COL3A1 overexpression rescues these effects, establishing the BNC2-COL3A1 axis as a critical driver of tumor progression. These findings highlight BNC2 as a potential biomarker and therapeutic target in pancreatic cancer, offering new insights into the molecular mechanisms underlying this aggressive disease.
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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.