title: [Role of glutathione S-transferase pi in tumor drug resistance].
abstract: OBJECTIVE
  To establish the cytologic expressing system for the glutathione S-transferase pi (GST-pi) cDNA.
  
  
  METHODS
  The pSV-GT, a recombinant plasmid containing rat GST-pi cDNA and the pSV-neo, a vector plasmid, were transfected the HeLa cells respectively and then G418 resistant colonies were isolated. The degree of the expression of GST-pi mRNA in the resultant cell lines was estimated by in situ hybridization using Digoxin-labelled probe cDNA. Cytotoxicity of variant anticancer drugs on the transfected cells were estimated by MTT assays.
  
  
  RESULTS
  Two subclones, HeLa/pSV-GT, and HeLa/pSV-neo, which transfected respectively by pSV-GT and pSV-neo, were established. HeLa/pSV-GT expressed significantly high degree of the GST-pi mRNA, where as both the HeLa/pSV-neo and the HeLa cell lines showed the similar but negligible degree of the GST-pi mRNA expression. Moreover, HeLa/pSV-GT cells were insensitive to adriamycin, mitomycin C, and cisplatinum as compared to HeLa/pSV-neo. Concentrations of adriamycin producing 50% inhibition (IC50) to HeLa/pSV-GT was 70.13 micrograms/ml, highly elevated 6.78-fold of that of HeLa/pSV-neo, to which IC50 was 10.34 micrograms/ml.IC50 of mitomycin and cisplatinum to HeLa/pSV-GT were 10.95 and 16.52 micrograms/ml respectively, slightly but significantly higher than those to HeLa/pSV-neo, which were 7.48 and 13.70 micrograms/ml. But the cytotoxicity of vincristine on the two cell lines were not significantly different.
  
  
  CONCLUSIONS
  These findings suggeste that HeLa/pSV-GT cell line, after being transfected with GST-pi cDNA, acquired drug-resistance property and the overexpression of GST-pi mRNA may contribute to the multidrug resistance of HeLa/pSV-GT cells. This cell line, as a stable cytogenetic system, will contribute more for the observation of GST-pi and drug resistance.
authors.affiliation: National Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, CAMS and PUMC, Beijing 100005.
authors.forename: W
authors.initials: W
authors.lastname: Cao
authors.forename: J
authors.initials: J
authors.lastname: Zuo
authors.forename: F
authors.initials: F
authors.lastname: Fang
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology; D002455:Cell Division / Q000187:drug effects; D002945:Cisplatin / Q000494:pharmacology; D018076:DNA, Complementary / Q000235:genetics; D004317:Doxorubicin / Q000494:pharmacology; D018432:Drug Resistance, Multiple; D019008:Drug Resistance, Neoplasm; D051549:Glutathione S-Transferase pi; D005982:Glutathione Transferase / Q000235:genetics*; D006367:HeLa Cells; D006801:Humans; D007527:Isoenzymes / Q000235:genetics*; D010957:Plasmids; D012333:RNA, Messenger / Q000235:genetics; D014162:Transfection
chemical_list: D000970:Antineoplastic Agents; D018076:DNA, Complementary; D007527:Isoenzymes; D012333:RNA, Messenger; D004317:Doxorubicin; C496556:GSTP1 protein, human; D051549:Glutathione S-Transferase pi; D005982:Glutathione Transferase; D002945:Cisplatin