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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 investigate the possible regulatory mechanism of HDPR1 (human homologue of Dapper) in the expression of p120ctn and β-catenin in lung cancer. Methods After silencing the expression of HDPR1 in lung cancer cell lines by siRNA, the expression of p120ctn and β-catenin were observed by RT-PCR and Western blot. The invasiveness of lung cancer cells was observed by Matrigel invasion assay. Results After silencing HDPR1 expression in lung cancer cell lines, the expression of p120ctn was significantly down-regulated while the expression of β-catenin was significantly up-regulated. The invasion ability of lung cancer cells was significantly enhanced. Conclusion The down-regulation of HDPR1 expression in lung cancer cells may promote the invasion ability of lung cancer cells by down-regulating the stability of p120ctn protein molecules and / or indirectly up-regulating the expression of β-catenin.