Genetics, structure, function, mode of actions and role in cancer development of CYP17

Anticancer Agents Med Chem. 2014 Jan;14(1):66-76. doi: 10.2174/187152061131300330.

Abstract

Most prostate and breast cancers are hormone dependent. The inhibition of steroid 17α-hydroxylase/17,20- lyase (CYP17), which is a crucial enzyme for steroid hormone biosynthesis, is widely used to treat androgen-dependent prostate cancer (PC). CYP17 has dual enzymatic activity: 17alpha-hydroxylase activity (utilizing delta4- C21 steroids as substrates) and the 17,20-lyase activity (using delta5- C21 steroids as substrates). The steroid biosynthetic pathway is directed to either the production of corticosteroids or sex hormones depending on the activity of CYP17. In this review, the current information on the genetics, molecular structure, substrate specificity and inhibitors of CYP17 is analyzed and discussed.

MeSH terms

  • Adrenal Cortex Hormones / biosynthesis
  • Androgens / biosynthesis
  • Breast Neoplasms / metabolism
  • Carcinogenesis / drug effects
  • Carcinogenesis / metabolism
  • Carcinogens, Environmental / metabolism
  • Carcinogens, Environmental / toxicity
  • Cytochromes b5 / metabolism
  • Female
  • Humans
  • Male
  • Neoplasms, Hormone-Dependent / metabolism
  • Prostatic Neoplasms / metabolism
  • Protein Conformation
  • Steroid 17-alpha-Hydroxylase / antagonists & inhibitors
  • Steroid 17-alpha-Hydroxylase / genetics*
  • Steroid 17-alpha-Hydroxylase / metabolism*
  • Substrate Specificity
  • Xenobiotics / metabolism
  • Xenobiotics / toxicity

Substances

  • Adrenal Cortex Hormones
  • Androgens
  • Carcinogens, Environmental
  • Xenobiotics
  • Cytochromes b5
  • Steroid 17-alpha-Hydroxylase