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Drug resistance effects of ribosomal protein L24 overexpression in hepatocellular carcinoma HepG2 cells.

作者信息

Guo Yong-Li, Kong Qing-Sheng, Liu Hong-Sheng, Tan Wen-Bin

机构信息

Oncology Department of the Jining First People's Hospital, Jining, Shandong, People's Republic of China E-mail :

出版信息

Asian Pac J Cancer Prev. 2014;15(22):9853-7. doi: 10.7314/apjcp.2014.15.22.9853.

DOI:10.7314/apjcp.2014.15.22.9853
PMID:25520117
Abstract

BACKGROUND

The morbidity and mortality rate of liver cancer continues to rise in China and advanced cases respond poorly to chemotherapy. Ribosomal protein L24 has been reported to be a potential therapeutic target whose 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 quantitative RT-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 null- transfected HepG2 cell lines.

RESULTS

The ribosomal protein L24 transcription level was 7.7 times higher in the drug-resistant HepG2 cells as compared to susceptible cells on quantitative RT-PCR analysis. This was associated 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 hepatocellular carcinoma HepG2 cells.

摘要

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