Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2004 Aug;51(3-4):146-53.
doi: 10.2152/jmi.51.146.

The p16INK4a-RB pathway: molecular link between cellular senescence and tumor suppression

Naoko Ohtani  1 , Kimi Yamakoshi, Akiko Takahashi, Eiji Hara
Affiliations
Free article
Review

The p16INK4a-RB pathway: molecular link between cellular senescence and tumor suppression

Naoko Ohtani et al. J Med Invest. 2004 Aug.
Free article

Abstract

The p16INK4a tumor suppressor protein functions as an inhibitor of CDK4 and CDK6, the D-type cyclin-dependent kinases that initiate the phosphorylation of the retinoblastoma tumor suppressor protein, RB. Thus, p16INK4a has the capacity to arrest cells in the G1-phase of the cell cycle and its probable physiological role is in the implementation of irreversible growth arrest termed cellular senescence. Cellular senescence is a state of permanent growth arrest that can be induced by a variety of stresses such as DNA-damage and aberrant mitogenic signaling in human primary cells. In contrast to normal cells, the function of the p16INK4a gene or its downstream mediators is frequently deregulated in many types of human cancers, illustrating the importance of cellular senescence in tumor suppression. Here we discuss the molecular mechanisms that direct cellular senescence and reveal its potential for tumor suppression.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

Substances