Jacquot C, Lanco X, Carbonnelle D, Sevestre O, Tomasoni C, Briad G, Juget M, Roussis V, Roussakis C
ISOMER Laboratory of Marine Pharmacology, Faculty of Pharmacy, Nantes, France.
Anticancer Res. 2002 Jul-Aug;22(4):2229-35.
Despite new protocols, non-small cell bronchopulmonary cancers are still difficult to treat by current chemotherapeutic procedures. Thus, it is essential to define new treatment strategies and detect new therapeutic targets. In order to define these new targets, this study applied the "differential display" (DD) technique to the NSCLC-N6 cell line treated with VT1 [methyl-4-methoxy-3-(3-methyl-2-butanoyl)benzoate]. VT1 induces arrest of the NSCLC-N6 cell cycle in the G1-phase, followed by cell death. DD enabled us to detect seven overexpressed mRNAs during treatment, four of which corresponded to identified genes: aldehyde dehydrogenase 1, nuclear transcription factor Nrfl, junctional adhesion molecule, and amino-ketobutyrate ligase. An antisense strategy showed that amino-ketobutyrate ligase is involved in the proliferation arrest of NSCLC-N6 cells in the G1-phase after VT1 treatment.
尽管有新的治疗方案,但非小细胞支气管肺癌目前仍难以通过化疗手段进行治疗。因此,确定新的治疗策略并检测新的治疗靶点至关重要。为了确定这些新靶点,本研究将“差异显示”(DD)技术应用于用VT1 [甲基-4-甲氧基-3-(3-甲基-2-丁酰基)苯甲酸酯]处理的NSCLC-N6细胞系。VT1诱导NSCLC-N6细胞周期在G1期停滞,随后细胞死亡。差异显示使我们能够检测到处理过程中七个过度表达的mRNA,其中四个对应于已鉴定的基因:醛脱氢酶1、核转录因子Nrfl、连接粘附分子和氨基酮丁酸连接酶。反义策略表明,氨基酮丁酸连接酶参与了VT1处理后NSCLC-N6细胞在G1期的增殖停滞。