目的研究HDPR1(human homologue of Dapper)在肺癌表达与p120ctn和β-catenin异常表达相关性的可能调节机制。方法运用siRNA技术沉默肺癌细胞系的HDPR1表达后,应用RT-PCR和Western blot技术观察p120ctn和β-catenin的表达情况,并应用基质胶侵袭实验观察肺癌细胞的侵袭能力。结果沉默肺癌细胞系中HDPR1表达后,p120ctn的表达明显下调,而β-catenin的表达明显上调,肺癌细胞的侵袭能力明显增强。结论肺癌细胞HDPR1的表达下调可通过下调p120ctn蛋白分子的稳定性和/或间接上调β-catenin的表达,从而促进肺癌细胞的侵袭能力。
Objective To explore the possible mechanism of human homologue of Dapper H (DPR1) gene on p120ctn and β-catenin expression, and on the invasive ability of lung cancer cells. Methods HDPR1 was knocked down using small interfering RNA (siRNA), RT-PCR and Western blotting were used to test the expression of p120ctn and β-catenin, and Matrigel invasion assay was used to examine the influence of HDPR1 on the invasiveness of lung cancer cells. Results The expression level of p120ctn protein was downregulated, β-catenin protein expression was upregulated and the invasive ability of lung cancer cells was increased after HDPR1 was knocked down in lung cancer cells. Conclusions HDPR1 gene knockdown enhances the invasion of lung cancer cells, probably related to downregulation of p120ctn and/or upregulatedβ-catenin expression.