Stemness and epithelial–mesenchymal transition (EMT) are two fundamental characteristics of metastasis that are controlled by diverse regulatory factors, including transcription factors. Compared with other subtypes of breast cancer, basal-type or triple-negative breast cancer (TNBC) has high frequencies of tumor relapse. However, the role of alpha-globin transcription factor CP2 (TFCP2) has not been reported as an oncogenic driver in those breast cancers. Here, we show that TFCP2 is a potent factor essential for EMT, stemness, and metastasis in breast cancer. TFCP2 directly bound promoters of EGF and TGFα to regulate their expression and stimulate autocrine signaling via EGFR. These findings indicate that TFCP2 is a new antimetastatic target and reveal a novel regulatory mechanism in which a positive feedback loop comprising EGF/TGFα and AKT can control malignant breast cancer progression. Significance: TFCP2 is a new antimetastatic target that controls TNBC progression via a positive feedback loop between EGF/TGFα and the AKT signaling axis.

中文翻译：

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包含EGF /TGFα的反馈环维持TFCP2介导的乳腺癌进展。

茎干和上皮间质转化（EMT）是转移的两个基本特征，受多种调控因素控制，包括转录因子。与其他亚型乳腺癌相比，基底型或三阴性乳腺癌（TNBC）的肿瘤复发频率较高。但是，尚未报道α-珠蛋白转录因子CP2（TFCP2）在这些乳腺癌中是致癌驱动力的作用。在这里，我们表明TFCP2是乳腺癌EMT，干性和转移必不可少的有效因子。TFCP2直接结合EGF和TGFα的启动子，以调节其表达并通过EGFR刺激自分泌信号传导。这些发现表明TFCP2是新的抗转移靶标，并揭示了一种新的调节机制，其中包括EGF /TGFα和AKT的正反馈回路可以控制恶性乳腺癌的进展。意义：TFCP2是一种新的抗转移目标，可通过EGF /TGFα与AKT信号轴之间的正反馈回路控制TNBC的进程。