Open AccessZNRF3 Inhibits the Invasion and Tumorigenesis in Nasopharyngeal Carcinoma Cells by Inactivating the Wnt/β-Catenin Pathway
Author(s) -
Zhongwei Wang,
Yali Wang,
Hongtao Ren,
Yingying Jin,
Ya Guo
Publication year - 2017
Publication title -
oncology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 57
eISSN - 1555-3906
pISSN - 0965-0407
DOI - 10.3727/97818823455816x14760478220149
Subject(s) - wnt signaling pathway , carcinogenesis , cancer research , nasopharyngeal carcinoma , cyclin d1 , ubiquitin ligase , biology , cell culture , ubiquitin , cell growth , cancer , signal transduction , cell cycle , microbiology and biotechnology , medicine , genetics , gene , radiation therapy
Zinc and ring finger 3 (ZNRF3), which belongs to the E3 ubiquitin ligase family, is involved in the progression and development of cancer. However, the expression and function of ZNRF3 in human nasopharyngeal carcinoma (NPC) remain unclear. Thus, the aim of this study was to investigate the role of ZNRF3 in human NPC. Our results showed that ZNRF3 was downregulated in NPC cell lines. Restoration of ZNRF3 significantly inhibited the proliferation of NPC cells and tumor xenograft growth in vivo. In addition, overexpression of ZNRF3 suppressed migration and invasion, as well as attenuated the epithelial-mesenchymal transition (EMT) process in NPC cells. Furthermore, restoration of ZNRF3 obviously downregulated the expression levels of β-catenin, cyclin D1, and c-Myc in NPC cells. In conclusion, these data suggest that ZNRF3 inhibited the metastasis and tumorigenesis via suppressing the Wnt/β-catenin signaling pathway in NPC cells. Thus, ZNRF3 may act as a novel molecular target for the treatment of NPC.