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Med Oncol (2015) 32:83DOI 10.1007/s12032-015-0539-5
ORIGINAL PAPER
VGLL4 inhibits EMT in part through suppressing Wnt/b-catenin signaling pathway in gastric cancer
Hui Li Ziwei Wang Wei Zhang
Kun Qian Gang Liao Wei Xu Shouru Zhang
Received: 7 January 2015 / Accepted: 13 February 2015 / Published online: 21 February 2015 Springer Science+Business Media New York 2015
Abstract VGLL4 is a member of the Vestigial-like proteins that functions as a tumor suppressor, which directly competes with YAP for binding TEADs in several cancer types. Recently, an increasing number of studies have reported that VGLL4 acts as a crucial role in regulating cell mobility, migration, and invasion. However, little is known about the signaling mechanisms in regulating epithelial mesenchymal transition (EMT) of gastric cancer. In our study, we conrmed that the expression level of VGLL4 was down-regulated in gastric cancer tissues, and reduced VGLL4 expression levels inhibited apoptosis and promoted proliferation, migration, and invasion. Additionally, we found a phenomenon that VGLL4 was associated with the change in nuclear location of b-catenin, which suggested that b-catenin was a signicant downstream factor of VGLL4. These results suggest that VGLL4 suppressed EMT in part via negative regulation of Wnt/b-catenin signaling pathway. Taken together, our study demonstrated that VGLL4 is important in the process of suppressing tumor progression of gastric cancer and provided a potential therapeutic strategy for gastric cancer.
Keywords VGLL4 Gastric cancer Wnt/b-catenin
Tumor progression EMT
Introduction
Gastric cancer is the fourth most frequent malignant neoplasm and the second leading cause of cancer death worldwide [1]. Invasiveness and metastasis are considered as a main reason for gastric cancer death. In the last few years, an increasing number of studies reported that epithelialmesenchymal transition (EMT) plays an important role in cancer progression and metastasis [24]. EMT is a process that is characterized by the loss of epithelial characteristics and acquisition of a mesenchymal pheno-type to produce enhanced motility, resistance to apoptosis, and the capacity to invade the surrounding tissues [58]. Many reports about EMT had been observed in various gastric cell lines such as MGC-803, MKN-45, SGC-7901, BGC-823 [9, 10]. It is well known that the occurrence of EMT is associated with several distinct pathways, including Notch, TGF-b, and several receptor tyrosine kinase [1113]. Furthermore, dysregulation of Wnt/b-catenin signaling has...