TG-interacting factor 1 (TGIF1) exerts inhibitory effects on transforming growth factor-beta (TGF-β) signaling by suppressing Smad signaling pathway at multiple levels. TGIF1 activity is important for normal embryogenesis and organogenesis, yet its dysregulation can culminate in tumorigenesis. For instance, increased expression of TGIF1 correlates with poor prognosis in triple-negative breast cancer patients, and enforced expression of TGIF1 facilitates Wnt-driven mammary tumorigenesis, suggesting that TGIF1 might function as an oncoprotein. Quite surprisingly, TGIF1 has recently been shown to function as a tumor suppressor in pancreatic ductal adenocarcinoma (PDAC), possibly owing to its ability to antagonize the pro-malignant transcription factor Twist1. In this article, we will briefly elaborate on the biological and clinical significance of the unique tumor-suppressive function of TGIF1 and its functional interaction with Twist1 in the context of PDAC pathogenesis and progression.

TG相互作用因子1（TGIF1）通过在多个水平上抑制Smad信号传导途径对转化生长因子-β（TGF-β）信号传导产生抑制作用。TGIF1活性对于正常的胚胎发生和器官发生很重要，但其失调可能最终导致肿瘤的发生。例如，TGIF1的表达增加与三阴性乳腺癌患者的不良预后相关，TGIF1的表达增强促进Wnt驱动的乳腺肿瘤发生，提示TGIF1可能起癌蛋白的作用。令人惊讶的是，TGIF1最近已显示出在胰腺导管腺癌（PDAC）中起抑癌作用，可能是由于它具有拮抗促恶性转录因子Twist1的能力。在这篇文章中，