Curcumin inhibits proliferation, invasion, angiogenesis and metastasis of different cancers through interaction with multiple cell signaling proteins

Cancer Lett. 2008 Oct 8;269(2):199-225. doi: 10.1016/j.canlet.2008.03.009. Epub 2008 May 13.

Abstract

Because most cancers are caused by dysregulation of as many as 500 different genes, agents that target multiple gene products are needed for prevention and treatment of cancer. Curcumin, a yellow coloring agent in turmeric, has been shown to interact with a wide variety of proteins and modify their expression and activity. These include inflammatory cytokines and enzymes, transcription factors, and gene products linked with cell survival, proliferation, invasion, and angiogenesis. Curcumin has been found to inhibit the proliferation of various tumor cells in culture, prevents carcinogen-induced cancers in rodents, and inhibits the growth of human tumors in xenotransplant or orthotransplant animal models either alone or in combination with chemotherapeutic agents or radiation. Several phase I and phase II clinical trials indicate that curcumin is quite safe and may exhibit therapeutic efficacy. These aspects of curcumin are discussed further in detail in this review.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Angiogenesis Inhibitors / pharmacology*
  • Animals
  • Antineoplastic Agents / pharmacology*
  • Breast Neoplasms / prevention & control
  • Cell Proliferation / drug effects
  • Clinical Trials as Topic
  • Curcumin / chemistry
  • Curcumin / pharmacokinetics
  • Curcumin / pharmacology*
  • Curcumin / therapeutic use
  • Gastrointestinal Neoplasms / prevention & control
  • Humans
  • Interleukins / antagonists & inhibitors
  • MAP Kinase Signaling System / drug effects
  • NF-kappa B / antagonists & inhibitors
  • Neoplasm Invasiveness
  • Neoplasm Metastasis / prevention & control
  • Neoplasms / drug therapy*
  • PPAR gamma / drug effects
  • STAT Transcription Factors / antagonists & inhibitors
  • Signal Transduction / drug effects*
  • Transcription Factor AP-1 / antagonists & inhibitors
  • Vascular Endothelial Growth Factor A / antagonists & inhibitors

Substances

  • Angiogenesis Inhibitors
  • Antineoplastic Agents
  • Interleukins
  • NF-kappa B
  • PPAR gamma
  • STAT Transcription Factors
  • Transcription Factor AP-1
  • Vascular Endothelial Growth Factor A
  • Curcumin