Biochemical and Biophysical Research Communications
Regular ArticleIncreased Sensitivity of Human Colon Cancer Cells to DNA Cross-Linking Agents after GRP78 Up-Regulation☆,☆☆,★
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2012, Pharmacology and TherapeuticsCitation Excerpt :ER preconditioning is achieved by pretreating cells with a sublethal concentration of an inducer of ER stress (e.g. thapsigargin, tunicamycin or dithiothreitol), which protects them from a subsequent ER insult by upregulating the UPR inhibitors Grp78 and Grp94 (Peyrou and Cribb, 2007) and by a p38-dependent process (Feng et al., 2011). In other cell systems, ER preconditioning drugs sensitize cells to other cytotoxic drugs (including cisplatin) (Belfi et al., 1999; Chatterjee et al., 1997; Chen et al., 2011; Gaddameedhi and Chatterjee, 2009; Xu et al., 2012) by a mechanism independent of Grp78, and apparently dependent on increased drug (cisplatin) accumulation (Budihardjo et al., 2000). This dual effect of ER preconditioning needs further exploration.
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These studies were supported in part by Grants CA63200 (N.A.B.) and R29 CA65920 (S.C.) from the National Cancer Institute, Public Health Service.
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Abbreviations used: AGT,O6-alkylguanine-DNA transferase; 6-AN, 6-aminonicotinamide; BCNU, 1,3-bis(2-dichloroethyl)-1-nitrosourea; CDDP, cisplatin; 2-dG, 2-deoxyglucose; ER, endoplasmic reticulum; GRP78, glucose-regulated stress protein; IC50, drug concentration that reduces colony formation or cell number by 50% relative to control; MEL, melphalan; MMR, mismatch repair; MNNG,N-methyl-N′-nitro-N-nitrosoguanidine; PARP, poly(ADP-ribose) polymerase; p(ADPR), poly(ADP-ribose); NER, nucleotide excision repair; SER, sensitizer enhancement ratio; Topo II, topoisomerase II; VP-16, etoposide.
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Nicoloff, J. A.Hoekstra, M. F.
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To whom correspondence should be addressed: BRB 301A, School of Medicine, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106-4937. Fax: 216-368-1166. E-mail:[email protected].