Drug Resistance Effects of Ribosomal Protein L24 Overexpression in Hepatocellular Carcinoma HepG2 Cells


Background: The morbidity and mortality rate of liver cancer continues to rise in China and advanced casesrespond poorly to chemotherapy. Ribosomal protein L24 has been reported to be a potential therapeutic targetwhose depletion or acetylation inhibits polysome assembly and cell growth of cancer. Materials and
Methods:Total RNA of cultured amycin-resistant and susceptible HepG2 cells was isolated, and real time quantitativeRT-PCR were used to indicate differences between amycin-resistant and susceptible strains of HepG2 cells.Viability assays were used to determine amycin resistance in RPL24 transfected and control vector and nulltransfectedHepG2 cell lines.
Results: The ribosomal protein L24 transcription level was 7.7 times higher inthe drug-resistant HepG2 cells as compared to susceptible cells on quantitative RT-PCR analysis. This wasassociated with enhanced drug resistance as determined by methyl tritiated thymidine (3H-TdR) incorporation.
Conclusions: The ribosomal protein L24 gene may have effects on drug resistance mechanisms in hepatocellularcarcinoma HepG2 cells.