FSCN1与钌配合物在抗胃癌中的作用及相关性研究

目的 探讨 FSCN1 在胃癌增殖中的作用,并研究FSCN1与钌配合物在胃癌中的相互作用. 方法 通过荧光定量PCR及Western blot法检测胃癌组织中FSCN1 的表达水平;MTT、EdU法检测干扰FSCN1后细胞增殖能力变化;用钌配合物处理SGC-7901后检测FSCN1 mRNA、蛋白表达水平及细胞的增殖能力;siRNA 抑制 FSCN1 的表达,过表达FSCN1后检测钌配合物对细胞的增殖能力影响. 结果 荧光定量PCR及Western blot法均显示胃癌组织中FSCN1 表达水平显著高于癌旁组织;MTT与EdU法结果显示,与siNC组比较,干扰 FSCN1 后细胞的增殖受到明显抑制( P <0. 01);钌配合物处理SGC-7901 后,定量PCR结果显示,与siNC组比较,FSCN1表达水平受到抑制(P<0. 01),MTT法结果显示,与siNC组比较,细胞增殖受到抑制( P<0. 01 );MMT法结果显示过表达FSCN1后抑制钌配合物对细胞增殖能力的影响. 结论 FSCN1具有促进胃癌细胞增殖的能力,钌配合物通过抑制FSCN1的表达起抑癌作用.

Ru complex as tumor inhibitor by regulating FSCN1 in gastric cancer cells

Objective To study the role of FSCN1 in the proliferation of gastric cancer and the interaction betweenFSCN1 and Ru complex in gastric cancer. Methods The expression level of FSCN1 was measured by qRTPCRand Western blot. The proliferation ability was tested using MTT and EdU assays. Then the mRNA and proteinlevels of FSCN1 in SGC-7901 cells were measured after treating with Ru complex. FSCN1 were transfected intocells, and the proliferation ability was tested using MTT and EdU assays after treating with Ru complex. ResultsThe expression level of FSCN1 in gastric cancer tissues was higher than that in adjacent tissues. Knockdown ofFSCN1 in SGC-7901 cells inhibited cell proliferation. The proliferation ability and the expression level of FSCN1 inSGC-7901 cells were decreased after treating with Ru complex. And overexpression of FSCN1 reversed the antitumoreffect of Ru complex. Conclusion FSCN1 as the oncogene can regulate gastric cancer proliferation, and Rucomplex reverses the course by inhibiting FSCN1 expression.