朱艳霞, 朱敬, 杨贤义, 肖敏. Krüppel样转录因子3在肺腺癌中表达的意义[J]. 中国肿瘤临床, 2012, 39(15): 1087-1090. DOI: 10.3969/j.issn.1000-8179.2012.15.023
引用本文: 朱艳霞, 朱敬, 杨贤义, 肖敏. Krüppel样转录因子3在肺腺癌中表达的意义[J]. 中国肿瘤临床, 2012, 39(15): 1087-1090. DOI: 10.3969/j.issn.1000-8179.2012.15.023
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Yan xia ZHU, Jing ZHU, Xian yi YANG, Min XIAO. Significance of Krüppel-like factor 3 Expression in Lung Adenocarcinoma[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2012, 39(15): 1087-1090. DOI: 10.3969/j.issn.1000-8179.2012.15.023
Citation: Yan xia ZHU, Jing ZHU, Xian yi YANG, Min XIAO. Significance of Krüppel-like factor 3 Expression in Lung Adenocarcinoma[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2012, 39(15): 1087-1090. DOI: 10.3969/j.issn.1000-8179.2012.15.023
shu

Krüppel样转录因子3在肺腺癌中表达的意义

Significance of Krüppel-like factor 3 Expression in Lung Adenocarcinoma

    摘要
  • 摘要:
      目的  探讨Krüippel样转录因子3(Krüippel-like factor 3, KLF3)在肺腺癌中的表达及其与临床特征的关系, 为探索KLF3在肺腺癌中的作用提供依据。
      方法  荧光定量PCR及Western blot分析KLF3的mRNA及蛋白在肺腺癌细胞株中的表达。收集72例肺腺癌患者的肿瘤组织标本, 免疫组织化学法分析KLF3在肺腺癌组织中表达并分析KLF3表达与患者临床特征的关系。
      结果  KLF3在肺腺癌细胞株中表达下调。大部分肺腺癌组织中KLF3低表达(50/72), 其表达主要定位于胞浆及胞核内。KLF3表达与肺腺癌临床病理分期(P < 0.000 1)及T分期(P=0.004)、N分期(P < 0.000 1)、M分期(P < 0.000 1)明显相关。
      结论  KLF3可能是一个重要的肺腺癌抑癌基因, 并有望成为新的抗肿瘤治疗靶点。

     

    Abstract:
      Objective  To investigate the expression of the Krüppel-like transcription factor 3 (Krüppel-like factor 3, KLF3) in lung adenocarcinoma (LAC) and its clinical features, which provides the basis for exploring the role of KLF3 in LAC.
      Methods  The mRNA and protein expression of KLF3 in LAC cell lines was analyzed by using quantitative polymerase chain reaction and Western blot analysis. A total of 72 LAC specimens from patients who were admitted to the Taihe Hospital, Hubei University of Medicine, Shiyan, between 2009 and 2011 were selected. Immunohistochemical staining was used for the analysis of KLF3 expression in the specimens, and an analysis of the correlation between KLF3 expression and the clinical features of patients with LAC was conducted.
      Results  KLF3 was down-regulated in the cancer cells and was decreased in a majority of LAC patients (50/72). Moreover, the KLF3 protein was primarily located in the cytoplasm and nucleus. KLF3 expression was found to be significantly correlated with the clinical pathological period (P < 0.0001), T stage (P = 0.004), N stage (P < 0.0001), and M stage (P < 0.0001) of LAC patients.
      Conclusion  KLF3 may be an important tumor suppressor gene in LAC and may thereby be a new anti-tumor therapeutic target.

     

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