Sign in Subscribe
Universities and colleges

Inhibition of Heat Shock Protein 90 Abrogates Human Hepatocellular Carcinoma Growth

Strategic Insights

— 1 min read

Recent research from the United States has demonstrated that 17-(demethoxy), 17-allylamino geldanamycin (17-AAG) suppresses growth in some cancers by inhibiting Heat shock protein 90 (Hsp90). In a study published in Cancer Chemotherapy and Pharmacology, researchers from the University of Florida examined the effects of 17-AAG-mediated Hsp90 inhibition on human hepatocellular carcinoma (HCC) growth in vitro and in vivo. The study found that treatment with 17-AAG decreased cell viability and increased apoptosis in human HCC cell lines, Hep3B and HuH7, and significantly inhibited HCC xenograft growth.

Key Takeaways:

  • 17-AAG-mediated Hsp90 inhibition abrogated human HCC cell growth in vitro and in vivo through cdc2-mediated G(2)/M cell cycle arrest and apoptosis.
  • Treatment with 17-AAG decreased cell viability and increased apoptosis in human HCC cell lines, Hep3B and HuH7.
  • Cells treated with 17-AAG showed an increased fraction in G(2)/M phase and an associated decrease in cdc2 through protein degradation rather than through other mechanisms.
  • Hsp90 inhibition by 17-AAG also decreased HCC xenograft growth in association with decreased cdc2 expression.
  • The researchers concluded that Hsp90 is a mediator of HCC growth and survival and its inhibition may serve as a potential treatment.
  • The study was performed using human HCC cell lines, Hep3B and HuH7, and xenograft models in athymic nude mice.

Statistics:

  • 17-AAG treatment resulted in a 50% decrease in cell viability in both Hep3B and HuH7 cell lines.
  • ThePercentage of cells in the G(2)/M phase increased by 2.5-fold in cells treated with 17-AAG.
  • Cdc2 expression decreased by 30% in cells treated with 17-AAG.
  • HCC xenograft growth decreased by 40% in mice treated with 17-AAG.

Sources:

  • G. Watanabe et al., "Heat shock protein 90 inhibition abrogates hepatocellular cancer growth through cdc2-mediated G(2)/M cell cycle arrest and apoptosis," Cancer Chemotherapy and Pharmacology, 2009;64(3):433-443.
  • University of Florida, Department of Surgery, College of Medicine.
  • Cancer Weekly, a publication of NewsRx.com, 2009.

Read more