癌症转移是导致近90%癌症患者死亡的主要原因。在消化系统中，恶性肿瘤常常转移到肝脏，比如胰腺导管腺癌（PDAC），有76 - 80%的患者会出现肝转移。科学家们注意到胚胎期的胰腺和肝脏都起源于内胚层，于是开始研究肝脏祖细胞中高表达的基因，是否会驱使PDAC细胞转移到肝脏。他们利用体外肝脏分化模型，找到了肝脏祖细胞中高表达的基因，其中TFAP2A在PDAC中高表达，并且和PDAC肝转移密切相关。原来，癌症相关成纤维细胞（CAFs）能通过骨形态发生蛋白4（BMP4）来提高TFAP2A的表达。功能实验显示，无论是在体外实验还是在动物体内实验中，TFAP2A的过度表达都会促进PDAC细胞的干性以及肝转移。从机制上来说，TFAP2A可以上调MYC，促进上皮 - 间质转化（EMT），还能招募巨噬细胞，帮助PDAC细胞进入血管，进而实现转移。这项研究揭示了PDAC肝转移的分子机制，也为找到潜在的治疗靶点提供了新方向。
期刊
iscience
标题
TFAP2A enhances tumor stemness and promotes metastasis in pancreatic ductal adenocarcinoma
作者
Jiaxin Luo, Zezhi Ding, Dongjie Chen, Yongsheng Jiang, Yizhi Cao, Minmin Shi, Xiaomei Tang, Jia Liu, Meilin Xue, Zehui Zhang, Kexian Li, Yu Bao, Fangfang Ma, Ting Wang, Lingxi Jiang
摘要
Metastasis is the leading cause of death for nearly 90% of patients with cancer. In the digestive system, malignancies preferentially metastasize to the liver, which occurs in 76–80% of patients with pancreatic ductal adenocarcinoma (PDAC). Given the shared endoderm origin of embryonic pancreas and liver, this study investigated whether genes highly expressed in liver progenitors drive PDAC cells metastasize to the liver. Using an in vitro liver differentiation model, genes highly expressed in liver progenitors were identified. Among them, TFAP2A was highly expressed in PDAC and closely related to PDAC liver metastasis. Cancer associated fibroblasts (CAFs) upregulated TFAP2A expression by bone morphogenetic protein 4 (BMP4). Functional experiments demonstrated that TFAP2A overexpression promoted PDAC cell stemness and liver metastasis in vitro and in vivo. Mechanistically, TFAP2A could promote epithelial mesenchymal transition (EMT) and recruit macrophage by upregulating MYC, facilitating PDAC cell intravasation. Collectively, these findings unveil molecular mechanisms for PDAC liver metastasis and potential therapeutic targets.
原文链接
https://www.cell.com/iscience/fulltext/S2589-0042(25)01321-5
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静远嘲风（MY Scimage） 成立于2007年，嘲风取自中国传统文化中龙生九子，子子不同的传说，嘲风为守护屋脊之瑞兽，喜登高望远；静远取自成语“宁静致远”，登高莫忘初心，远观而不可务远。
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