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<p>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.</p>

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BNC2 as a novel driver of pancreatic cancer progression through transcriptional regulation of COL3A1 and epithelial-to-mesenchymal transition

  • 期刊论文

  • 发表日期：

    2025年11月21日

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  • Xiuming Li,
  • Teng Yu,
  • Zien Yu,
  • Xun Zou,
  • Jingliang He,
  • Dan Wang,
  • Xiaozhu Shen,
  • Shunfang Liu,
  • Bin Liu

摘要

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.