title: [Effects of AS1411 on the apoptosis of taxol-resistant lung adenocarcinoma A549 cell].
abstract: OBJECTIVE
  To explore the effects of AS1411 on the apoptosis of taxol-resistant lung adenocarinoma A549 cell (A549/T cell).
  
  
  METHODS
  A549/T cells were treated with AS1411 at a concentration gradient of 0-20.0 µmol/L. The assays of methyl tolyl sulfide (MTS) and colony formation were used to detect the cellular vitality (absorbance value (A490 nm)) and proliferation. The apoptotic effects were detected by flow cytometer and the relevant apoptotic signaling proteins detected by Western blot.
  
  
  RESULTS
  A549/T cells exhibited some characteristics of epithelial mesenchymal transition (EMT) and a negative expression of epidermal growth factor receptor (EGFR). After a treatment of 5.0 µmol/L AS1411, compared to the control sequence, cell vitality was inhibited (A490 nm: 0.185 ± 0.009 vs 0.272 ± 0.006, P < 0.001) and the number of clone formation decreased (74 ± 13 vs 120 ± 12, P = 0.010). With rising AS1411 concentration, A549/T cells vitality decreased in a dose-dependent manner. After a 48-hour treatment of 20.0 µmol/L AS1411, the ratio of apoptosis ((19.9 ± 2.6)%) had significant difference (P = 0.002) with the control sequence group ((8.8 ± 1.3)%). Compared to the control sequence group, the expressions of protein kinase B (AKT), extracellular regulated protein kinases 1/2 (ERK1/2) and B-cell lymphoma 2 (Bcl-2) protein declined (0.353 ± 0.003, 0.432 ± 0.015, 0.294 ± 0.015 vs 0.688 ± 0.003, 0.911 ± 0.019, 0.422 ± 0.018, all P < 0.001).
  
  
  CONCLUSIONS
  AS1411 may induce the apoptosis of A549/T cells through inhibiting the AKT-ERK pathways.
authors.affiliation: State Key Laboratory of Molecular Oncology, Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Zhou
authors.affiliation: State Key Laboratory of Molecular Oncology, Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.
authors.forename: Zitong
authors.initials: Z
authors.lastname: Zhao
authors.affiliation: State Key Laboratory of Molecular Oncology, Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.
authors.forename: Lingyan
authors.initials: L
authors.lastname: Liu
authors.affiliation: State Key Laboratory of Molecular Oncology, Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.
authors.forename: Qimin
authors.initials: Q
authors.lastname: Zhan
authors.affiliation: State Key Laboratory of Molecular Oncology, Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China. Email: symlh2006@163.com.
authors.forename: Yongmei
authors.initials: Y
authors.lastname: Song
mesh_terms: D000230:Adenocarcinoma / Q000473:pathology*; D000077192:Adenocarcinoma of Lung; D017209:Apoptosis / Q000187:drug effects; D052157:Aptamers, Nucleotide; D045744:Cell Line, Tumor; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D006801:Humans; D008175:Lung Neoplasms / Q000473:pathology*; D009838:Oligodeoxyribonucleotides / Q000494:pharmacology*; D017239:Paclitaxel / Q000494:pharmacology*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D015398:Signal Transduction
chemical_list: C513936:AGRO 100; D052157:Aptamers, Nucleotide; D009838:Oligodeoxyribonucleotides; D019253:Proto-Oncogene Proteins c-bcl-2; D051057:Proto-Oncogene Proteins c-akt; D048049:Extracellular Signal-Regulated MAP Kinases; D017239:Paclitaxel