中文摘要：

目的研究凝溶胶蛋白（gelsolin，GSN）对雌激素受体α（ERα）阳性、人表皮生长因子受体2（Her2）过表达乳腺癌细胞MCF7／Her2生长的作用。方法构建GSN的真核表达载体，并稳定转染MCF7／Her2细胞，以RT-PCR及WesternBlot鉴定得到稳定过表达GSN的乳腺癌细胞系McF7／Her2／GsN。以空载体转染的稳定表达细胞MCF7／Her2／V作对照，比较其细胞形态、增殖和迁移能力的改变；WesternBlot及RT-PCR检测Her2、组织金属蛋白酶抑制剂-3（TIMP3）表达和细胞外调节蛋白激酶（ERK）的活化，探索深层次的作用机制。结果MCF7／Her2稳定过表达GSN后，细胞形态改变且增殖及迁移、侵袭能力明显低于对照细胞；发现Her2表达下降，TIMP3的表达上调，而雌激素导致的MCF7／Her2细胞ERK活化增强被逆转。结论凝溶胶蛋白能降低Her2的表达，并通过下调ERK的活化及上调TIMP3的表达，抑制乳腺癌细胞MCF7／Her2增殖及迁移侵袭作用。

英文摘要：

Objective To study the function of gelsolin （GSN） in ERa positive, Her2 high expression breast cancer cell MCFT/Her2. Methods Constructed a gelsolin expression plasmid. Established a gelsolin stable - overexpression cell line by stable transfection with hygromycin selection. The cell line was identified of the GSN overexpression by RT -PCR and Western Blot. Cell morphology, cell growth and ability of migration/invasion of GSN overexpression cell line were compared to the control vector transfected ceils and the parental cell line. Her2, TIMP3 expression and the ERK activation were studied by real -time RT -PCR and Western Blot. Re- suits Cell morphology of GSN overexpression cells was changed and the proliferation and migration/invasion were inhibited in GSN overexprssion cells. Conclusion Gelsolin may inhibit the proliferation and migration/invasion of MCFT/Her2 cells by reducing expression of Her2, increasing expression of TIMP3 and inhibiting the ERα non - genomic activity. It is demonstrated that GSN can reverse the proliferation and migration/invasion caused by Her2.