p53 but not p16(INK4a) induces growth arrest in retinoblastoma-deficient hepatocellular carcinoma cells

Morel A., Unsal K., ÇAĞATAY T., Ponchel F., Carr B., Ozturk M.

JOURNAL OF HEPATOLOGY, vol.33, no.2, pp.254-265, 2000 (SCI-Expanded) identifier

  • Publication Type: Article / Article
  • Volume: 33 Issue: 2
  • Publication Date: 2000
  • Doi Number: 10.1016/s0168-8278(00)80366-9
  • Journal Name: JOURNAL OF HEPATOLOGY
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.254-265
  • Keywords: cell cycle arrest, cyclin E, hepatoma, p16(INK4a), p21(Cip1), p53, retinoblastoma, VIRUS-X PROTEIN, TUMOR-SUPPRESSOR, FUNCTIONAL INACTIVATION, CYCLE INHIBITION, APOPTOSIS, GENE, MUTANT, ASSOCIATION, EXPRESSION, MUTATION
  • Istanbul University Affiliated: Yes

Abstract

Background/Aim: Both p16(INK4a) and p53 proteins are negative regulators of the cell cycle. In human hepatocellular carcinomas (HCC), the loss of function of p53, retinoblastoma (pRb) and p16(INK4a) genes by different mechanisms has been largely documented, but their hepatocellular effects are poorly known, We compared the growth-inhibitory effects of p16(INK4a) and p53 proteins in Hep3B cell line-derived clones.