Abstract
BackgroundMetastasis remains the major cause of death in nasopharyngeal carcinoma (NPC). Yippee-like 3 (YPEL3) plays an important role in tumorigenesis. However, its function and mechanism in NPC has not been systematically explored.MethodsWe evaluated YPEL3 expression in NPC cell lines and tissues using real-time PCR and western blotting. Then, we established NPC cell lines that stably overexpressed YPEL3 and knocked down YPEL3 expression to explore its function in NPC in vitro and in vivo. Additionally, we investigated the potential mechanism of YPEL3 action by identifying the Wnt/β-catenin signaling pathway downstream genes using western blotting.ResultsYPEL3 was downregulated in NPC cell lines and tissue samples. Ectopic expression of YPEL3 inhibited NPC cell migration and invasion in vitro; while silencing of YPEL3 promoted NPC cell migration and invasion. Further study indicated that overexpression of YPEL3 inhibited NPC cell epithelial–mesenchymal transition (EMT) and that silencing it enhanced EMT. Overexpression of YPEL3 suppressed NPC cell lung metastasis in vivo. The mechanism study determined that YPEL3 suppressed the expression levels of Wnt/β-catenin signaling pathway downstream genes and the nuclear translocation of β-catenin.ConclusionsYPEL3 suppresses NPC EMT and metastasis by suppressing the Wnt/β-catenin signaling pathway, which would help better understanding the molecular mechanisms of NPC metastasis and provide novel therapeutic targets for NPC treatment.
Highlights
Metastasis remains the major cause of death in nasopharyngeal carcinoma (NPC)
Recent studies have found that murine Yippee-like 3 (YPEL3) is related to cell growth inhibition through apoptosis, which is involved in the programmed cell death of murine myeloid precursor cells during differentiation [7, 10]
Compared to NP69 cells, YPEL3 was significantly downregulated in the NPC cell lines at both mRNA and protein level (Fig. 1a, b)
Summary
Metastasis remains the major cause of death in nasopharyngeal carcinoma (NPC). Nasopharyngeal carcinoma (NPC) is a head and neck cancer with a high prevalence rate (20–50 cases per 100,000 people) in South China [1, 2]. Intensitymodulated radiotherapy and chemotherapy have improved the local control, distant metastasis remains the major cause of death in NPC [3, 4]. Recent studies have found that murine YPEL3 is related to cell growth inhibition through apoptosis, which is involved in the programmed cell death of murine myeloid precursor cells during differentiation [7, 10]. The roles and mechanism of YPEL3 in NPC development and progression remain unclear
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