Comprehensive analyses for the mechanism of PIVKA-II production from hepatocellular carcinoma

PIVKA-II广泛应用于肝细胞癌（HCC）临床，但PIVKA-II产生的确切机制仍不清楚。我们已经证明，PIVKA-II是在HCC成为转移表型（上皮间质转化：EMT）时产生的，该表型通过肌动蛋白重排损害维生素K的摄取。在这个项目中，我们证明了进一步的EMT会导致肝脏特异性蛋白质合成受损，导致PIVKA-II生产受损，即使HCC仍然生长。此外，增强超声检查的结果与手术切除的肝癌中PIVKA-II的产生密切相关。综上所述，PIVKA-II可能是HCC的生物学标志物以及HCC的肿瘤标志物。

PIVKA-II is generally used in hepatocellular carcinoma (HCC) clinic, but precise mechanism of PIVKA-II production is still unkown. We have demonstrated that PIVKA-II was produced when HCC became metastatic phenotype (epithelial mesenchymal transition: EMT) that was impaired uptake of vitamin K by actin rearrangement. In this project, we demonstrated that further EMT caused impairment of liver specific protein synthesis, resulting in impairment of PIVKA-II production even though HCC still grew. Moreover, findings in enhanced ultrasonography well-correlated with PIVKA-II production in surgically resected HCC. Taken together, PIVKA-II could be an biological marker for HCC as well as a tumor marker of HCC.