Overexpression of aldose reductase in liver cancers may contribute to drug resistance

K. W.Y. Lee, Chi Bun Ko, Z. Jiang, D. Cao, S. S.M. Chung

Research output: Journal article publicationJournal articleAcademic researchpeer-review

76 Citations (Scopus)


We previously found that about 29% of human liver cancers overexpressed aldose reductase (AR) and about 54% of them overexpressed an AR-like gene called ARL-1 that has similar enzymatic activities to AR. Since these aldo-keto reductases can reduce a broad spectrum of substrates including cytotoxic aldehydes, we were interested to find out if these enzymes can contribute to the resistance of liver cancer chemotherapy by inactivating some of the anticancer drugs. HepG2 cells, a stable line of liver cells, were induced to overexpress AR by hypertonicity. Cells that were cultured in hypertonic medium became more resistant to daunorubicin, suggesting that ovarexpression of AR made the cells more resistant to this drug. This is confirmed by the fact that addition of AR inhibitor sensitizes the cells to this drug again. This information may be important for designing new drugs to treat this deadly disease.
Original languageEnglish
Pages (from-to)129-132
Number of pages4
JournalAnti-Cancer Drugs
Issue number2
Publication statusPublished - 22 Mar 2001
Externally publishedYes


  • Aldose reductase
  • Daunorubicin
  • Drug resistance
  • Hepatocellular carcinoma
  • Liver cancer

ASJC Scopus subject areas

  • Oncology
  • Pharmacology
  • Pharmacology (medical)
  • Cancer Research


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