ER-α36过表达促进人乳腺癌MCF-7细胞侵袭转移能力

 目的 探讨雌激素受体新亚型ER-α36过表达对人雌激素受体阳性乳腺癌细胞侵袭转移潜力的影响及其机制。方法 以野生型乳腺癌细胞系MCF-7/W、转染pcDNA3.1空载体的细胞系MCF-7/pcDNA3.1和转染重组载体pcDNA3.1/ER-α36的细胞系MCF-7/ER-α36为研究对象，分别用细胞粘附实验观测肿瘤细胞与细胞外基质的粘附能力、Transwell侵袭小室实验检测细胞侵袭转移能力，用Western blot法检测NF-κB P65、MMP-2、MMP-9和TIMP-1蛋白表达。结果 与MCF-7/W组细胞相比，MCF-7/ ER-α36细胞的2h细胞粘附率和24h穿膜细胞数显著增加(P<0.05)。NF-κB P65、MMP-2、MMP-9和TIMP-1蛋白的相对表达量及MMP-2/TIMP-1、MMP-9/TIMP-1显著增高（P<0.05）。结论 ER-α36过表达能促进ER-α66阳性乳腺癌细胞的体外粘附能力和侵袭转移潜力，其机制可能与通过NF-κ B途径提高MMP-2、MMP-9的表达水平及打破二者与TIMP-1之间的平衡有关。

Over-expression of estrogen receptor-alpha 36 promotes the invasion and metastasis ability of human breast cancer cell MCF-7

Objective To explore the effect of ER-α36, a novel variant of estrogen receptor α, on the invasion and metastasis potential in the human estrogen receptor-positive cell and its mechanism. Methods Wild type breast cancer cell line MCF-7 (MCF-7/W), MCF-7 cells transfected with pcDNA3.1 empty vector cells (the MCF-7/pcDNA3), MCF-7 cells transfected with the recombinant vector pcDNA3.1/ER-α36 cells (the MCF-7/ ER-α36) were the research objects. The adhesion between tumor cells and extracellular matrix was observed by cell adhesion test. The cell invasion and metastasis was detected by Transwell chamber experiments. The expression levels of NF-κB P65, MMP-2, MMP-9, and TIMP-1 were analysed by Western blot. MCF-7 / ER-α36 cells. Results Compared with MCF-7 / W group, the adhesion rate after growing 2h and the number of penetrating cells after growing 24h were increased had significant differences (P <0.05). The Western blot analysis results showed that the relative expression level of NF-κ P65, MMP-2, MMP-9, TIMP-1 and MMP- 2/TIMP-1, MMP-9/TIMP-1 in MCF-7/ERα36 group had a significant difference (P <0.05). Conclusions ER-α36 can promote the ability of the cell invasion and metastasis potential in the ER-α66-positive breast cancer cells. The mechanism possibly is ralated with increasing the expression level of MMP-9 and MMP-2 through NF-κB pathway, and breaking the balance between this and TIMP-1.