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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

YPEL3 suppressed lung metastasis in vivo. Nude BALB/C mice were intravenously injected via the tail vein with SUNE-1 cells stably overexpression YPEL3 or vector (n = 9 in each group). a Representative images of macroscopic lung metastases, arrowheads indicate the metastatic nodes; b Quantification of the average number of macroscopic metastatic nodes formed on the lung surface; c Representative images of HE staining (×100); d Quantification of the average number of microscopic metastatic nodes formed in the lungs based on pathological analysis of HE-stained sections. Data presented are the mean ± SD; **P < 0.01 compared with control using Student t-test
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Fig5: YPEL3 suppressed lung metastasis in vivo. Nude BALB/C mice were intravenously injected via the tail vein with SUNE-1 cells stably overexpression YPEL3 or vector (n = 9 in each group). a Representative images of macroscopic lung metastases, arrowheads indicate the metastatic nodes; b Quantification of the average number of macroscopic metastatic nodes formed on the lung surface; c Representative images of HE staining (×100); d Quantification of the average number of microscopic metastatic nodes formed in the lungs based on pathological analysis of HE-stained sections. Data presented are the mean ± SD; **P < 0.01 compared with control using Student t-test

Mentions: To determine the role of YPEL3 in NPC cell metastasis in vivo, we constructed a lung metastasis model by injecting SUNE-1 cells stably overexpressing YPEL3 or vector into the tail veins of nude mice. After 8 weeks, fewer macroscopic metastatic nodes were seen on the lung surfaces of the YPEL3-overexpressing group as compared with the vector group (Fig. 5a, b). In addition, there were smaller and fewer microscopic metastatic nodules in the YPEL3-overexpressing group than in the vector group (Fig. 5c, d). These results indicate that YPEL3 suppresses NPC cell metastasis, suggesting YPEL3 functions as a negative regulator of metastasis.Fig. 5


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)

YPEL3 suppressed lung metastasis in vivo. Nude BALB/C mice were intravenously injected via the tail vein with SUNE-1 cells stably overexpression YPEL3 or vector (n = 9 in each group). a Representative images of macroscopic lung metastases, arrowheads indicate the metastatic nodes; b Quantification of the average number of macroscopic metastatic nodes formed on the lung surface; c Representative images of HE staining (×100); d Quantification of the average number of microscopic metastatic nodes formed in the lungs based on pathological analysis of HE-stained sections. 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

Fig5: YPEL3 suppressed lung metastasis in vivo. Nude BALB/C mice were intravenously injected via the tail vein with SUNE-1 cells stably overexpression YPEL3 or vector (n = 9 in each group). a Representative images of macroscopic lung metastases, arrowheads indicate the metastatic nodes; b Quantification of the average number of macroscopic metastatic nodes formed on the lung surface; c Representative images of HE staining (×100); d Quantification of the average number of microscopic metastatic nodes formed in the lungs based on pathological analysis of HE-stained sections. Data presented are the mean ± SD; **P < 0.01 compared with control using Student t-test
Mentions: To determine the role of YPEL3 in NPC cell metastasis in vivo, we constructed a lung metastasis model by injecting SUNE-1 cells stably overexpressing YPEL3 or vector into the tail veins of nude mice. After 8 weeks, fewer macroscopic metastatic nodes were seen on the lung surfaces of the YPEL3-overexpressing group as compared with the vector group (Fig. 5a, b). In addition, there were smaller and fewer microscopic metastatic nodules in the YPEL3-overexpressing group than in the vector group (Fig. 5c, d). These results indicate that YPEL3 suppresses NPC cell metastasis, suggesting YPEL3 functions as a negative regulator of metastasis.Fig. 5

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