title: hTERT gene expression levels and telomerase activity in drug resistant MCF-7 cells.
abstract: OBJECTIVE
  Cancer cells and some highly proliferative normal cells can stabilize telomere lengths by telomerase, which adds hexameric repeats to the ends of linear chromosomes. In this study, the activity of telomerase reverse transcriptase (hTERT) and its gene expression levels were investigated in paclitaxel, docetaxel, vincristine and doxorubicin resistant human MCF-7 breast adenocarcinoma cells.
  
  
  METHODS
  Resistant cell lines were developed by stepwise selection of cells (MCF-7/S) in increasing doses of paclitaxel (MCF-7/Pac), docetaxel (MCF-7/Doc), vincristine (MCF-7/Vinc) and doxorubicin (MCF-7/Dox). Antiproliferative effects of anticancer drugs were evaluated by XTT assay and IC 50 values for different drugs were determined from cell proliferation curves. Expression levels of hTERT gene in sensitive and resistant cells were analyzed by RT-PCR. TRAP-Silver Staining assay was used to evaluate telomerase activities in these cells.
  
  
  RESULTS
  When drug resistant and sensitive MCF-7 cells were compared no significant differences were observed in hTERT expression levels and telomerase enzyme activities.
  
  
  CONCLUSIONS
  This report demonstrates that drug resistance developed against paclitaxel, docetaxel, vincristine and doxorubicin in MCF-7 cells is independent of the expression of hTERT gene and telomerase activity.
authors.affiliation: Middle East Technical University, Department of Biological Sciences, Ankara, Turkey.
authors.forename: V
authors.initials: V
authors.lastname: Sakin
authors.forename: U
authors.initials: U
authors.lastname: Eskiocak
authors.forename: M D
authors.initials: MD
authors.lastname: Kars
authors.forename: O D
authors.initials: OD
authors.lastname: Iseri
authors.forename: U
authors.initials: U
authors.lastname: Gunduz
mesh_terms: D000903:Antibiotics, Antineoplastic / Q000494:pharmacology; D000970:Antineoplastic Agents / Q000494:pharmacology; D000972:Antineoplastic Agents, Phytogenic / Q000494:pharmacology; D001943:Breast Neoplasms / Q000188:drug therapy / Q000201:enzymology / Q000235:genetics*; D049109:Cell Proliferation / Q000187:drug effects*; D000077143:Docetaxel; D004317:Doxorubicin / Q000494:pharmacology; D019008:Drug Resistance, Neoplasm; D005260:Female; D015971:Gene Expression Regulation, Enzymologic / Q000502:physiology*; D006801:Humans; D017239:Paclitaxel / Q000494:pharmacology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012334:RNA, Neoplasm / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D043823:Taxoids / Q000494:pharmacology; D019098:Telomerase / Q000235:genetics / Q000378:metabolism*; D014407:Tumor Cells, Cultured; D014750:Vincristine / Q000494:pharmacology
chemical_list: D000903:Antibiotics, Antineoplastic; D000970:Antineoplastic Agents; D000972:Antineoplastic Agents, Phytogenic; D012333:RNA, Messenger; D012334:RNA, Neoplasm; D043823:Taxoids; D000077143:Docetaxel; D014750:Vincristine; D004317:Doxorubicin; C509186:TERT protein, human; D019098:Telomerase; D017239:Paclitaxel