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Human p14(ARF)-mediated cell cycle arrest strictly depends on intact p53 signaling pathways

  1. Author:
    Weber, H. O.
    Samuel, T.
    Rauch, P.
    Funk, J. O.

  2. Author Address

    Univ Erlangen Nurnberg, Dept Dermatol, Lab Mol Tumor Biol, Hartmannstr 14, D-91052 Erlangen, Germany Univ Erlangen Nurnberg, Dept Dermatol, Lab Mol Tumor Biol, D-91052 Erlangen, Germany NCI, Regulat Cell Growth Lab, Frederick, MD 21702 USA Funk JO Univ Erlangen Nurnberg, Dept Dermatol, Lab Mol Tumor Biol, Hartmannstr 14, D-91052 Erlangen, Germany
    1. Year: 2002
  2. Journal: Oncogene
    1. 21
    2. 20
    3. Pages: 3207-3212
  4. Type of Article: Article
  1. Abstract:

    The tumor suppressor ARF is transcribed from the INK4a/ARF locus in partly overlapping reading frames with the CDK inhibitor p16(Ink4a). ARF is able to antagonize the MDM2- mediated ubiquitination and degradation of p53, leading to either cell cycle arrest or apoptosis, depending on the cellular context. However, recent data point to additional p53- independent functions of mouse p19(ARF). Little is known about the dependency of human p14(ARF) function on p53 and its downstream genes. Therefore, we analysed the mechanism of p14(ARF)-induced cell cycle arrest in several human cell types. Wild-type HCT116 colon carcinoma cells (p53(+/+)p21(CIP1+/+) 14-3-3sigma(+/+)), but not p53(-/-) counterparts, underwent G(1) and G(2) cell cycle arrest following infection with a p14(ARF)-adenovirus. In p21(CIP1-/-) cells, p14(ARF) did not induce G(1) or G(2) arrest, while 14-3-3sigma(-/-) counterparts were mainly arrested in G(1), pointing to essential roles of p21(CIP1) in G(1) and G(2) arrest and cooperative roles of p21 and 14-3-3sigma in ARF-mediated G(2) arrest. Our data demonstrate a strict p53 and p21(CIP1) dependency of p14(ARF)- induced cell cycle arrest in human cells.

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