肿瘤干细胞是肿瘤复发与转移的机制之一。上皮-间质转化（EMT）是肿瘤转移的起始。申请人前期研究证实PIWIL2为乳腺癌独立预后因素；在EMT化乳腺癌干细胞中PIWIL2和piR-932表达增高，二者结合后发挥正向调节EMT的生物学作用。因此，我们设想：PIWIL2和piR-932可能通过促进乳腺癌细胞EMT而诱导其获得“干性”，甚至转变为乳腺癌干细胞。为证实该设想，课题组拟通过临床标本、乳腺癌细胞系和动物模型，分析PIWIL2和piR-932表达的临床意义，研究PIWIL2和piR-932对乳腺癌干细胞的调控作用及机制，明晰PIWIL2和piR-932诱导乳腺癌细胞获得“干性”甚至转变为乳腺癌干细胞的生物学过程。本课题以乳腺癌干细胞为研究对象，以其来源为切入点，系统研究PIWIL2和piR-932对乳腺癌干细胞的作用及机制，为乳腺癌干细胞的来源提供理论依据，为乳腺癌的靶向治疗寻找靶点。

Breast cancer stem cells might play an important role in metastasis or recurrence of breast cancer. Epithelial-mesenchymal transition (EMT) is thought to be the beginning of metastasis. In our previous research, we found that up-expression of PIWIL2 in breast cancer which suggests poor prognosis. We also found that PIWIL2 and piR-932 have regulating effect on EMT of breast cancer stem cells. With references and our work, we propose the hypothesis: PIWI2/piR-932 could induce stemness transformation in breast cancer cells by promoting EMT. To prove that, we use clinical samples to observe the correlation between PIWIL2/piR-932 and EMT signal with prognosis or recurrence of breast cancer. Furthermore, we separate non-stemness CD44-CD24+ cancer cells, over-express PIWIL2/piR-932 in the cells, and observe whether the EMT and stemness transformation are improved. On the contrary, we interfere the expression of PIWIL2 and piR-932, and watch changes of EMT, the metastasis ability and stem cell markers in CD44+CD24- cancer cells. We comprehensively regulate Latexin expression to investigate the effect on stemness maintenance in breast cancer stem cells. This study will offer potential target and evidence for breast-cancer-stem-cell-targeting therapy from the point of PIWIL2/piR-932.