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, cilt.33, sa.2, ss.254-265, 2000 (SCI-Expanded) identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 33 Sayı: 2
  • Basım Tarihi: 2000
  • Doi Numarası: 10.1016/s0168-8278(00)80366-9
  • Dergi Adı: JOURNAL OF HEPATOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.254-265
  • Anahtar Kelimeler: 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
  • İstanbul Üniversitesi Adresli: Evet

Özet

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.