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Riboregulator H19 induction of MDR1-associated drug resistance in human hepatocellular carcinoma cells.

Author information

Affiliations

  • 1. Department of Biochemistry, The Chinese University of Hong Kong, Shatin, Hong Kong SAR, China.
      Authors
    • Tsang WP 1
    (1 author)

Oncogene, 05 Feb 2007, 26(33):4877-4881
https://doi.org/10.1038/sj.onc.1210266 PMID: 17297456 

Abstract 

Acquisition of drug resistance is one of the main obstacles encountered in cancer chemotherapy. Overexpression of multi-drug resistance 1 (MDR1) gene and its protein product P-glycoprotein, accompanied with a decrease in doxorubicin accumulation level, was observed in doxorubicin-resistant R-HepG2 cells, a subline derived by selection of human hepatocellular carcinoma HepG2 cells with doxorubicin. In addition, Northern-blot analysis revealed an eight fold upregulation of the imprinted H19 mRNA in R-HepG2 cells. H19 knockdown by transfection with antisense H19 oligonucleotides suppressed the MDR1/P-glycoprotein expression, increased the cellular doxorubicin accumulation level and sensitized doxorubicin toxicity in both HepG2 parent cells and R-HepG2 cells. Results from methylation-specific polymerase chain reaction analysis indicated that the MDR1 gene promoter was hypomethylated in R-HepG2 cells. Antisense H19 oligonucleotides transfection induced a marked increase in the percentage of MDR1 promoter methylation and decrease in MDR1 expression in R-HepG2 cells. Thus, the H19 gene is believed to induce P-glycoprotein expression and MDR1-associated drug resistance at least in liver cancer cells through regulation of MDR1 promoter methylation.

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Read article at publisher's site: https://doi.org/10.1038/sj.onc.1210266

Read article for free, from open access legal sources, via Unpaywall: https://www.nature.com/articles/1210266.pdfUnpaywall

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