关键词: 乳腺癌, 雌激素受体-α 36, MCF-7细胞系, 侵袭转移, 核因子-κ B

Abstract: 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.

Key words: breast cancer, estrogen receptor alpha 36, MCF-7 cell line, invasion and metastasis, nuclear factor kappa B