Background: Over-expression of P-glycoprotein (Pgp) is associated with liver cancer development from HBV . Glycoprotein synthesis in malignant tissues is limited by Dolichyl Phosphate (DolP). The aim of the present study was to investigate the effect of polyprenol (PP) which provides a DolP substitute in regulation of N-glycosylation on Pgp over-expression in the development of liver cancer in HBV infection. Methods Human hepatocytes, infected with HBV and human hepatocarcinoma HEP 3B cell line were used. Pgp was assessed by an immunohistochemical technique. DolP fractions were analysed by HPLC methods. Results It is confirmed that plasmatic membrans of hepatocytes cells contain 7,9 -9,4% of Pgp (the total protein amount) as a resistance marker. HBV infected cells differ from normal hepatocytes in Pgp content by 4-5 times and HEP 3B cells differ by 10-12 times The study showed 5-fold DolP decrease in HBV infected cells and 10-fold DolP decrease in HEP3B cells. The investigations demonstrate that the situation can be changed by treatment with DolP and PP. The DolP concentration in HBV infected hepatocytes was returned to the normal level. It is established that DolP in the concentration 10 -6 M aid 6-8-fold reducing Pgp in membranes of HBV infected cells. Background: Metastasis is one of the most complicated and major pathological processes responsible for poor prognosis of hepatocellular carcinoma. Snail was recently highlighted as a critical transcriptional factor for tumor metastasis. Method & Result: Real time RT/PCR and Western blot analysis demonstrated that Snail mRNA and protein, respectively, were induced by 12-Otetradecanoylphorbol-13-acetate (TPA) in hepatoma cell HepG2. Blockade of gene expression of Snail by antisense oligodeoxynucleotide and/or siRNA technique can prevent not only the TPA-triggered EMT/cell migration and growth inhibition of HepG2 but also TPA-induced down-regulation of E-cadherin and up-regulation of p15INK4b. Moreover, the TPA-triggered promoter activation of p15INK4b was also prevented. On the other hand, two of the HepG2 clone overexpressing Snail, namely S7 and S15, had a scattered fibroblastic morphology and acquired higher motility than parental HepG2. Also, the proportion of G0/G1 phase of S7 and S15 was higher than that of parental HepG2, consistent with the longer doubling time of both cells. Semiquantitative RT/PCR analysis demonstrated a greatly elevated gene expression of Snail accompanied with decreased E-cadherin and increased p15INK4b in both Snail-overexpressing cells. On the transcriptional level, p15INK4b promoter activity was 2.6-fold higher in S7 as compared with parental HepG2. Furthermore, electrophoretic mobility of DNA fragments encompassing proximal p15INK4b promoter can be retarded by incubation of nuclear extract of S7. Conclusion: Our results demonstrated that Snail play diverse trans-regulatory roles in HepG2. Notably, we suggested that Snail may upregulate p15INK4b gene expression by directly activating its promoter.