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Overexpression of p21 WAF1/CIP1 induces cell differentiation and growth inhibition in a human glioma cell line
Author(s) -
Kokunai Takashi,
Izawa Ichiro,
Tamaki Norihiko
Publication year - 1998
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19980209)75:4<643::aid-ijc24>3.0.co;2-8
Subject(s) - cyclin dependent kinase , biology , cellular differentiation , cell growth , microbiology and biotechnology , glioma , cyclin , cell culture , cancer research , kinase , cell cycle , differentiation therapy , cell cycle checkpoint , cell , gene , genetics , acute promyelocytic leukemia , retinoic acid
p21 WAF1/CIP1 is a downstream mediator of p53 and mediates growth arrest by inhibiting the action of G 1 cyclin‐dependent kinases. Since cellular differentiation is frequently characterized by G 1 arrest, we examined whether p21 WAF1/CIP1 overexpression would induce growth suppression and differentiation in p53 ‐defective human glioma cells. Overexpression of p21 WAF1/CIP1 resulted in an accumulation of cells in G 1 , altered morphology, growth arrest and cell differentiation. The extent of cell differentiation correlated with the level of p21 WAF1/CIP1 as well as of proliferating cell nuclear antigen, cyclin E, and cdk 2, which associates with p21 WAF1/CIP1 . Our data suggest that gene transfer of p21 WAF1/CIP1 may arrest glioma cell growth in vivo by committing malignant glioma cells to a pathway of terminal differentiation. Int. J. Cancer 75:643–648, 1998. © 1998 Wiley‐Liss, Inc.