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Article: Failure to dephosphorylate retinoblastoma protein in drug-resistant cells

TitleFailure to dephosphorylate retinoblastoma protein in drug-resistant cells
Authors
Issue Date1995
Citation
Cancer Research, 1995, v. 55 n. 22, p. 5222-5225 How to Cite?
AbstractHypophosphorylation of retinoblastoma protein (RB) accompanies the DNA damage-induced, p53-independent G1 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 cell 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.
Persistent Identifierhttp://hdl.handle.net/10722/194104
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDou, QP-
dc.contributor.authorLui, VWY-
dc.date.accessioned2014-01-30T03:32:10Z-
dc.date.available2014-01-30T03:32:10Z-
dc.date.issued1995-
dc.identifier.citationCancer Research, 1995, v. 55 n. 22, p. 5222-5225-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/194104-
dc.description.abstractHypophosphorylation of retinoblastoma protein (RB) accompanies the DNA damage-induced, p53-independent G1 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 cell 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.-
dc.languageeng-
dc.relation.ispartofCancer Research-
dc.titleFailure to dephosphorylate retinoblastoma protein in drug-resistant cells-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid7585579-
dc.identifier.scopuseid_2-s2.0-0028882740-
dc.identifier.volume55-
dc.identifier.issue22-
dc.identifier.spage5222-
dc.identifier.epage5225-
dc.identifier.isiWOS:A1995TD88700021-

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