# Differential Associations of PIVKA-II with Epithelial and Mesenchymal Features in HCC and PDAC

## TL;DR

This study explores how PIVKA-II relates to EMT features in HCC and PDAC, suggesting it may play a role in tumor progression and could be a useful diagnostic marker.

## Contribution

The study reveals a context-dependent role for PIVKA-II in EMT processes in HCC and PDAC, offering new insights into tumor biology and diagnostics.

## Key findings

- PIVKA-II shows dual roles in HCC and PDAC, linking to EMT markers and tumor invasiveness.
- E-cadherin is selectively detected in HCC, indicating limited EMT activation.
- Vimentin is more highly expressed in PDAC, reflecting a stronger EMT shift.

## Abstract

Hepatocellular carcinoma (HCC) and pancreatic ductal adenocarcinoma (PDAC) are aggressive malignancies characterized by a poor prognosis and resistance to conventional therapies. Mounting evidence suggests the pivotal role of epithelial–mesenchymal transition (EMT) in tumor progression, metastasis, and therapeutic resistance in these cancers. Protein induced by vitamin K absence II (PIVKA-II)—a valuable HCC detector—has ultimately emerged as a potentially relevant biomarker in PDAC, serving as both a serum biomarker and a prognostic indicator. This study investigates the putative link between PIVKA-II expression and the EMT process in HCC and PDAC. Using a Western blot analysis and electrochemiluminescence immunoassay (ECLIA), we quantified PIVKA-II serum levels alongside two canonical EMT markers—Vimentin and E-cadherin—in selected cohorts. Emerging data suggest a dual, context-dependent role for PIVKA-II. Beyond its diagnostic value in both malignancies, its co-expression with EMT markers points to a potential mechanistic involvement in tumor invasiveness and phenotypic plasticity. Notably, the selective detection of E-cadherin in HCC implies limited EMT activation and a preservation of the epithelial phenotype, whereas the higher expression of Vimentin in PDAC reflects a more substantial shift toward EMT. We provide a comprehensive analysis of key molecular markers, their involvement in EMT-driven pathophysiological mechanisms, and their potential as novel diagnostic tools.