ArticleInternational journal of molecular sciences2024
PANC-1 Cell Line as an Experimental Model for Characterizing PIVKA-II Production, Distribution, and Molecular Mechanisms Leading to Protein Release in PDAC.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 7 citations in OpenAlex.
- Protein Induced by Vitamin K Absence or Antagonist II in Primary Liver Cancer: Basic Research Insights and Clinical Applications.Journal of clinical and translational hepatology · 2025Review
- Characterization of PIVKA-II Molecular Forms via Size Exclusion Chromatography and Hydrophobic Interaction Chromatography in HCC Patients.Journal of clinical laboratory analysis · 2025Article
- Establishing a Decision-Making Threshold for PIVKA II in the Diagnosis of Pancreatic Ductal Adenocarcinoma (PDAC): A Single Centre Experience.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Differential Associations of PIVKA-II with Epithelial and Mesenchymal Features in HCC and PDAC.International journal of molecular sciences · 2025Article
- Recent Developments of 1,3,4-Thiadiazole Compounds as Anticancer Agents.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Elevated Serum Protein Induced by Vitamin K Absence or Antagonist II Levels in Patients with Hepatic Hemangiomas.International journal of molecular sciences · 2025Article
- Article
- Emerging horizons on molecular and circulating biomarkers in pancreatic adenocarcinoma.Frontiers in oncology · 2024Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) represents a highly aggressive malignancy with a lack of reliable diagnostic biomarkers. Protein induced by vitamin K absence (PIVKA-II) is a protein increased in various cancers (particularly in hepatocellular carcinoma), and it has recently exhibited superior diagnostic performance in PDAC detection compared to other biomarkers. The aim of our research was to identify an in vitro model to study PIVKA-II production, distribution, and release in PDAC. We examined the presence of PIVKA-II protein in a panel of stabilized pancreatic cancer cell lines by Western blot analysis and indirect immunofluorescence (IFA). After quantitative evaluation of PIVKA-II in PaCa 44, H-Paf II, Capan-1, and PANC-1, we adopted the latter as a reference model. Subsequently, we analyzed the effect of glucose addiction on PIVKA-II production in a PANC-1 cell line in vitro; PIVKA-II production seems to be directly related to an increase in glucose concentration in the culture medium. Finally, we evaluated if PIVKA-II released in the presence of increasing doses of glucose is concomitant with the expression of two well-acknowledged epithelial-mesenchymal transition (EMT) markers (Vimentin and Snail). According to our experimental model, we can speculate that PIVKA-II release by PANC-1 cells is glucose-dependent and occurs jointly with EMT activation.
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