Keratin 17 upregulation promotes cell metastasis and angiogenesis in colon adenocarcinoma.
Keratin 17 upregulation promotes cell metastasis and angiogenesis in colon adenocarcinoma.
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DOI：
10.1080/21655979.2021.2010393
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发表时间：
2021-12
期刊：
影响因子：
4.9
通讯作者：
Liu Z
中科院分区：
文献类型：
--
作者：
Ji R;Ji Y;Ma L;Ge S;Chen J;Wu S;Huang T;Sheng Y;Wang L;Yi N;Liu Z
结肠腺癌(COAD)是结肠癌的主要病理类型，恶性程度高，预后差。此前的研究表明角蛋白17（KRT17）在许多恶性肿瘤的发生发展中发挥着重要作用。然而，COAD 的作用和分子机制仍不清楚。使用TCGA和ONCOMINE数据库以及免疫组织化学，我们发现COAD组织中KRT17的表达高于邻近正常组织。细胞和动物实验表明，KRT17的过度表达促进了结肠癌细胞的侵袭和转移，而敲除KRT17则在体外和体内逆转了这些过程。此外，我们还表明KRT17促进新血管的形成。从机制上讲，KRT17可以调节WNT/β-catenin信号通路，APC可能通过与KRT17相互作用参与这一过程。总之，这些发现表明KRT17的高表达可以通过调节WNT/β-catenin信号通路促进结肠癌细胞的细胞转移和血管生成。因此，KRT17可能是COAD治疗的潜在治疗靶点。
Colon adenocarcinoma (COAD), having high malignancy and poor prognosis, is the main pathological type of colon cancer. Previous studies show that Keratin 17 (KRT17) plays an important role in the development of many malignant tumors. However, its role and the molecular mechanism underlying COAD remain unclear. Using TCGA and ONCOMINE databases, as well as immunohistochemistry, we found that the expression of KRT17 was higher in COAD tissues as compared to that in the adjacent normal tissues. Cell- and animal-based experiments showed that overexpression of KRT17 promoted the invasion and metastasis of colon cancer cells while knocking down KRT17 reversed these processes both in vitro and in vivo. In addition, we also showed that KRT17 promoted the formation of new blood vessels. Mechanistically, KRT17 could regulate the WNT/β-catenin signaling pathway, and APC may be involved in this process by interacting with KRT17. In summary, these findings suggested that high expression of KRT17 could promote cell metastasis and angiogenesis of colon cancer cells by regulating the WNT/β-catenin signaling pathway. Thus, KRT17 could be a potential therapeutic target for COAD treatment.
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