Overexpression of p21waf1 leads to increased inhibition of E2F-1 phosphorylation and sensitivity to anticancer drugs in retinoblastoma-negative human sarcoma cells

Cancer Res. 1997 Jun 1;57(11):2193-9.

Abstract

The effect of overexpression of p21waf1 on drug sensitivity was studied in an osteosarcoma cell line (SaOs-2) lacking both p53 and functional retinoblastoma protein using a tetracycline (TC)-inducible expression system. p21waf1 expression was barely detectable in SaOS-2 cells incubated in the presence of TC. After TC withdrawal, high levels of p21waf1 were induced in these cells. These p21waf1-induced cells showed increased sensitivity to doxorubicin, tomudex, and methotrexate as compared to uninduced cells; this condition is associated with increased apoptosis. Expression of p21waf1 reduced cyclin A-associated kinase activity and, surprisingly, resulted in inhibition of phosphorylation of E2F-1 and increased E2F-1 binding activity. An S-G2 cell cycle arrest/delay and an increase in expression of E2F-responsive genes (dihydrofolate reductase and thymidylate synthase) was correspondingly observed. Overexpression of p21waf1 in cells lacking functional retinoblastoma protein may mediate sensitivity to anticancer drugs by inhibiting E2F-1 phosphorylation, which may contribute to increased S-G2 cell cycle delay and increased cell susceptibility to apoptosis.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Anti-Bacterial Agents / pharmacology
  • Antibiotics, Antineoplastic / pharmacology
  • Antimetabolites, Antineoplastic / pharmacology
  • Apoptosis
  • Carrier Proteins*
  • Cell Cycle / genetics
  • Cell Cycle / physiology
  • Cell Cycle Proteins*
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclin-Dependent Kinases / metabolism
  • Cyclins / genetics*
  • Cyclins / metabolism*
  • DNA-Binding Proteins*
  • Doxorubicin / pharmacology
  • E2F Transcription Factors
  • E2F1 Transcription Factor
  • Gene Expression Regulation, Neoplastic
  • Genes, p53
  • Humans
  • Methotrexate / pharmacology
  • Osteosarcoma / drug therapy*
  • Osteosarcoma / genetics*
  • Osteosarcoma / metabolism
  • Phosphorylation
  • Quinazolines / pharmacology
  • Retinoblastoma Protein / metabolism
  • Retinoblastoma-Binding Protein 1
  • Tetracycline / pharmacology
  • Tetrahydrofolate Dehydrogenase / genetics
  • Thiophenes / pharmacology
  • Thymidylate Synthase / genetics
  • Transcription Factor DP1
  • Transcription Factors / metabolism*
  • Tumor Cells, Cultured

Substances

  • Anti-Bacterial Agents
  • Antibiotics, Antineoplastic
  • Antimetabolites, Antineoplastic
  • CDKN1A protein, human
  • Carrier Proteins
  • Cell Cycle Proteins
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins
  • DNA-Binding Proteins
  • E2F Transcription Factors
  • E2F1 Transcription Factor
  • E2F1 protein, human
  • Quinazolines
  • Retinoblastoma Protein
  • Retinoblastoma-Binding Protein 1
  • Thiophenes
  • Transcription Factor DP1
  • Transcription Factors
  • Doxorubicin
  • Tetrahydrofolate Dehydrogenase
  • Thymidylate Synthase
  • Cyclin-Dependent Kinases
  • Tetracycline
  • raltitrexed
  • Methotrexate