Failure to Dephosphorylate Retinoblastoma Protein in Drug-resistant Cells

Q. Ping Dou, Vivian W.Y. Lui

Research output: Contribution to journalArticlepeer-review

30 Scopus citations


Hypophosphorylation of retinoblastoma protein (RB) accompanies the DNA damage-induced, p53-independent Gt arrest and apoptosis in two p53-null human leukemic cell lines, HL-60 and U937 (Q. P. Dou et aL, Proc Natl. Acad. Sci. USA, 92:9019-9023,1995). When an HL-60 ceU line resistant to cytosine arabinoside was exposed to this DNA-damaging agent, neither RB hypophosphorylation nor apoptosis were observed. In contrast, treatment of these cells with another DNA-damaging agent, etoposide, dramatically induced these events, which were inhibitable by the addition of zinc chloride, a protein tyrosine phosphatase inhibitor. Induction of hypophosphorylation of RB may be an important novel strategy for treating drug-resistant cancers.

Original languageEnglish (US)
Pages (from-to)5222-5225
Number of pages4
JournalCancer Research
Issue number22
StatePublished - Nov 15 1995
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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