Tumor suppressor $p16^{INK4a}$ in Cancer

  • Lee, Mee-Hyun (National Research Laboratory of Molecular Carcinogenesis and Chemoprevention, College of Pharmacy, Seoul National University.) ;
  • Choi, Bu-Young (Laboratory of Molecular Biology, C&C Research Labs) ;
  • Surh, Young-Joon (National Research Laboratory of Molecular Carcinogenesis and Chemoprevention, College of Pharmacy, Seoul National University.)
  • 이미현 (서울대학교 약학대학, 발암기전 및 분자암예방 국가지정 연구실) ;
  • 최부영 (C&C 신약연구소) ;
  • 서영준 (서울대학교 약학대학, 발암기전 및 분자암예방 국가지정 연구실)
  • Published : 2005.09.01

Abstract

[ $p16^{INK4a}$ ] is a tumor suppressor that belongs to the INK4 family of the cyclin D-dependent kinases (cdk) inhibitors. It plays regulatory roles in cell proliferation and in tumorigenesis by interacting with Rb signaling. Abnormally elevated $p16^{INK4a}$ protein expression causes cell cycle arrest (G1/S transition) and loss of cyclin-cdk activity. In many cancers, $p16^{INK4a}$ is altered by mutation, deletion, and promoter methylation. This review summarizes the function of p16 as an important regulator of cancer pathobiology and a promising target fer developing cancer therapeutic and chemopreventive agents.

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