CYP3A4 intronic SNP rs35599367 (CYP3A4*22) alters RNA splicing

Pharmacogenet Genomics. 2016 Jan;26(1):40-3. doi: 10.1097/FPC.0000000000000183.

Abstract

Cytochrome P450 3A4 (CYP3A4) metabolizes 30-50% of clinically used drugs. Large interperson variability in CYP3A4 activity affects response to CYP3A4 substrate drugs. We had demonstrated that an intronic single nucleotide polymorphism rs35599367 (CYP3A4*22, located in intron 6) reduces mRNA/protein expression; however, the underlying mechanism remained unknown. Here we show that CYP3A4*22 is associated with a two-fold or greater increase in formation of a nonfunctional CYP3A4 alternative splice variant with partial intron 6 retention in human liver (P=0.006), but not in small intestines. Consistent with this observation, in-vitro transfection experiments with a CYP3A4 minigene (spanning from intron 5 to intron 7) demonstrated that plasmids carrying the rs35599367 minor T allele caused significantly greater intron 6 retention than the C allele in liver derived HepG2 cells, but not in intestine-derived LS-174T cells. These results indicate that tissue-specific increased formation of nonfunctional alternative splice variant causes reduced CYP3A4 mRNA/protein expression in CYP3A4*22 carriers.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Cell Line
  • Cytochrome P-450 CYP3A / genetics*
  • Hep G2 Cells
  • Humans
  • Intestines / cytology
  • Introns*
  • Liver / cytology
  • Organ Specificity
  • Polymorphism, Single Nucleotide*
  • RNA Splicing*
  • RNA, Messenger / metabolism

Substances

  • RNA, Messenger
  • Cytochrome P-450 CYP3A
  • CYP3A4 protein, human