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YPEL3 suppresses epithelial-mesenchymal transition and metastasis of nasopharyngeal carcinoma cells through the Wnt/β-catenin signaling pathway.

Zhang J, Wen X, Ren XY, Li YQ, Tang XR, Wang YQ, He QM, Yang XJ, Sun Y, Liu N, Ma J - J. Exp. Clin. Cancer Res. (2016)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Sun Yat-sen University Cancer Center; State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, 651 Dongfeng Road East, Guangzhou, People's Republic of China.

ABSTRACT

Background: Metastasis 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.

Methods: We 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.

Results: YPEL3 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.

Conclusions: YPEL3 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.

No MeSH data available.


Related in: MedlinePlus

Effects of YPEL3 overexpression on NPC cell migration and invasion in vitro. a Representative western blotting analysis of YPEL3 overexpression in CNE-2 and SUNE-1 cells. GAPDH served as the loading control. b-d Representative images and quantification of the effects of YPEL3 overexpression on the migratory and invasive abilities of CNE-2 and SUNE-1 cells as determined by wound healing (b), Transwell migration (c), and invasion (d) assays. All of the experiments were performed at least three times. Data presented are the mean ± SD; **P < 0.01 compared with control using Student t-test
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Fig2: Effects of YPEL3 overexpression on NPC cell migration and invasion in vitro. a Representative western blotting analysis of YPEL3 overexpression in CNE-2 and SUNE-1 cells. GAPDH served as the loading control. b-d Representative images and quantification of the effects of YPEL3 overexpression on the migratory and invasive abilities of CNE-2 and SUNE-1 cells as determined by wound healing (b), Transwell migration (c), and invasion (d) assays. All of the experiments were performed at least three times. Data presented are the mean ± SD; **P < 0.01 compared with control using Student t-test

Mentions: To study whether YPEL3 affects the migratory and invasive abilities of NPC cells, we performed wound healing, Transwell migration, and invasion assays using CNE-2 and SUNE-1 cells stably overexpressing YPEL3 or vector. As shown in Fig. 2a, Western blotting validated that YPEL3 protein level was obviously elevated after stably overexpressing YPEL3 in NPC cells. The wound healing assay demonstrated that the migratory ability of CNE-2 and SUNE-1 cells stably overexpressing YPEL3 was much lower than that of cells expressing vector plasmid (Fig. 2b). Overexpressing YPEL3 suppressed the migratory (Fig. 2c) and invasive (Fig. 2d) abilities of the NPC cells as determined by the Transwell migration and invasion assays. These findings indicate that YPEL3 inhibits the migratory and invasive abilities of NPC cells in vitro.Fig. 2


YPEL3 suppresses epithelial-mesenchymal transition and metastasis of nasopharyngeal carcinoma cells through the Wnt/β-catenin signaling pathway.

Zhang J, Wen X, Ren XY, Li YQ, Tang XR, Wang YQ, He QM, Yang XJ, Sun Y, Liu N, Ma J - J. Exp. Clin. Cancer Res. (2016)

Effects of YPEL3 overexpression on NPC cell migration and invasion in vitro. a Representative western blotting analysis of YPEL3 overexpression in CNE-2 and SUNE-1 cells. GAPDH served as the loading control. b-d Representative images and quantification of the effects of YPEL3 overexpression on the migratory and invasive abilities of CNE-2 and SUNE-1 cells as determined by wound healing (b), Transwell migration (c), and invasion (d) assays. All of the experiments were performed at least three times. Data presented are the mean ± SD; **P < 0.01 compared with control using Student t-test
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4940860&req=5

Fig2: Effects of YPEL3 overexpression on NPC cell migration and invasion in vitro. a Representative western blotting analysis of YPEL3 overexpression in CNE-2 and SUNE-1 cells. GAPDH served as the loading control. b-d Representative images and quantification of the effects of YPEL3 overexpression on the migratory and invasive abilities of CNE-2 and SUNE-1 cells as determined by wound healing (b), Transwell migration (c), and invasion (d) assays. All of the experiments were performed at least three times. Data presented are the mean ± SD; **P < 0.01 compared with control using Student t-test
Mentions: To study whether YPEL3 affects the migratory and invasive abilities of NPC cells, we performed wound healing, Transwell migration, and invasion assays using CNE-2 and SUNE-1 cells stably overexpressing YPEL3 or vector. As shown in Fig. 2a, Western blotting validated that YPEL3 protein level was obviously elevated after stably overexpressing YPEL3 in NPC cells. The wound healing assay demonstrated that the migratory ability of CNE-2 and SUNE-1 cells stably overexpressing YPEL3 was much lower than that of cells expressing vector plasmid (Fig. 2b). Overexpressing YPEL3 suppressed the migratory (Fig. 2c) and invasive (Fig. 2d) abilities of the NPC cells as determined by the Transwell migration and invasion assays. These findings indicate that YPEL3 inhibits the migratory and invasive abilities of NPC cells in vitro.Fig. 2

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Sun Yat-sen University Cancer Center; State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, 651 Dongfeng Road East, Guangzhou, People's Republic of China.

ABSTRACT

Background: Metastasis 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.

Methods: We 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.

Results: YPEL3 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.

Conclusions: YPEL3 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.

No MeSH data available.


Related in: MedlinePlus