Breast cancer is a common type of cancer in females. Our previous studies indicated that leucine aminopeptidase 3 (LAP3) promotes migration and invasion of breast cancer cells. Vimentin is a mesenchymal marker, and its upregulation represents the promotion of epithelial–mesenchymal transition. In this study, we found that LAP3 and vimentin were highly expressed in breast cancer tissues, and the overexpression of LAP3 in breast cancer cells promoted the expression of vimentin. Western blot analysis indicated that the overexpression of LAP3 upregulated the phosphorylation of Erk1/2. MEK inhibitor PD98059 downregulated the expression of vimentin, matrix metalloproteinase-2/9 (MMP-2/9), and fascin through the inhibition of Erk1/2 activity. We hypothesized that LAP3 promoted tumor migration and invasion by upregulating vimentin. The knockdown of vimentin resulted in the inhibited migration and invasion of MDA-MB-231 and MDA-MB-468 cells. The expression of MMP-2/9 and fascin could also be downregulated. In conclusion, vimentin might play an important role in the promotion of breast cancer metastasis by LAP3.

乳腺癌是女性常见的癌症类型。我们之前的研究表明亮氨酸氨肽酶 3 (LAP3) 促进乳腺癌细胞的迁移和侵袭。波形蛋白是间充质标志物，其上调代表促进上皮间质转化。本研究发现LAP3和波形蛋白在乳腺癌组织中高表达，而LAP3在乳腺癌细胞中的过表达促进了波形蛋白的表达。蛋白质印迹分析表明，LAP3 的过表达上调了 Erk1/2 的磷酸化。MEK 抑制剂 PD98059 通过抑制 Erk1/2 活性下调波形蛋白、基质金属蛋白酶-2/9 (MMP-2/9) 和肌成束蛋白的表达。我们假设 LAP3 通过上调波形蛋白促进肿瘤迁移和侵袭。波形蛋白的敲低导致 MDA-MB-231 和 MDA-MB-468 细胞的迁移和侵袭受到抑制。MMP-2/9 和肌成束蛋白的表达也可能被下调。总之，波形蛋白可能在LAP3促进乳腺癌转移中起重要作用。