Implications of hedgehog signaling antagonists for cancer therapy

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

The hedgehog (Hh) pathway, initially discovered in Drosophila by two Nobel laureates, Dr. Eric Wieschaus and Dr. Christiane Nusslein-Volhard, is a major regulator for cell differentiation, tissue polarity and cell proliferation. Studies from many laboratories, including ours, reveal activation of this pathway in most basal cell carcinomas and in approximately 30% of extracutaneous human cancers, including medulloblastomas, gastrointestinal, lung, breast and prostate cancers. Thus, it is believed that targeted inhibition of Hh signaling may be effective in treating and preventing many types of human cancers. Even more exciting is the discovery and synthesis of specific signaling antagonists for the Hh pathway, which have significant clinical implications in novel cancer therapeutics. This review discusses the major advances in the current understanding of Hh signaling activation in different types of human cancers, the molecular basis of Hh signaling activation, the major antagonists for Hh signaling inhibition and their potential clinical application in human cancer therapy.

Original languageEnglish (US)
Pages (from-to)670-680
Number of pages11
JournalActa Biochimica et Biophysica Sinica
Volume40
Issue number7
DOIs
StatePublished - Jul 2008
Externally publishedYes

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Hedgehogs
Chemical activation
Neoplasms
Therapeutics
Cell proliferation
Medulloblastoma
Gastrointestinal Neoplasms
Basal Cell Carcinoma
Drosophila
Cells
Cell Differentiation
Lung Neoplasms
Prostatic Neoplasms
Tissue
Cell Proliferation
Breast Neoplasms

Keywords

  • Antagonist
  • Basal cell carcinoma
  • Hedgehog
  • Human cancer therapy
  • PTCH1
  • Smoothened

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics

Cite this

Implications of hedgehog signaling antagonists for cancer therapy. / Xie, Jingwu.

In: Acta Biochimica et Biophysica Sinica, Vol. 40, No. 7, 07.2008, p. 670-680.

Research output: Contribution to journalArticle

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