Basal type breast cancer is the most aggressive and has mesenchymal features with a high metastatic ability. However, the signaling node that determines the basal type features in breast cancer remains obscure. Here, we report that FYN among SRC family kinases is required for the maintenance of basal type breast cancer subtype. Importantly, FYN enhanced NOTCH2 activation in basal type breast cancer cells through STAT5-mediated upregulation of Jagged-1 and DLL4 NOTCH ligands, thereby contributed to mesenchymal phenotypes. In addition, we found that high levels of FYN persist in basal type breast cancer cells by a positive feedback loop between FYN and STAT5. FYN interacted directly with STAT5 and increased p-STAT5 that further acts as a transcription factor for FYN. Taken together, our findings demonstrate a pivotal role of FYN and its downstream effectors in maintaining the basal type features in breast cancer.

中文翻译：

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FYN通过STAT5 / NOTCH2信号节点促进基础型乳腺癌细胞的间充质表型。

基底型乳腺癌是最具有侵略性的，具有具有高转移能力的间质特征。但是，决定乳腺癌基础类型特征的信号转导节点仍然不清楚。在这里，我们报告说，SRC家族激酶之间的FYN是维持基础型乳腺癌亚型所必需的。重要的是，FYN通过STAT5介导的Jagged-1和DLL4 NOTCH配体的上调增强了基础型乳腺癌细胞中的NOTCH2活化，从而促进了间充质表型。此外，我们发现，通过FYN和STAT5之间的正反馈回路，高水平的FYN持续存在于基础型乳腺癌细胞中。FYN直接与STAT5相互作用，并增加了p-STAT5，后者进一步充当FYN的转录因子。在一起