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MiR200-upregulated Vasohibin 2 promotes the malignant transformation of tumors by inducing epithelial-mesenchymal transition in hepatocellular carcinoma.

Xue X, Zhang Y, Zhi Q, Tu M, Xu Y, Sun J, Wei J, Lu Z, Miao Y, Gao W - Cell Commun. Signal (2014)

Bottom Line: VASH2 knockdown in HepG2 cells inhibited epithelial-mesenchymal transition (EMT), but VASH2 overexpression in Hep3B cells promoted EMT.Western blot analyses showed that VASH2 promoted EMT through the ZEB1/2 pathway.VASH2 promoted invasion, reduced apoptosis and increased the proportion of stem cells in vitro and in vivo.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, the First Affiliated Hospital with Nanjing Medical University, 300# Guangzhou Road, Nanjing, 210029, China. xfxue@suda.edu.cn.

ABSTRACT

Background: Hepatocellular carcinoma (HCC) typically relies on tumor transformation and angiogenesis for its malignant behavior, including growth and metastasis. Previously, we reported that Vasohibin2 (VASH2) is preferentially expressed in hepatocellular carcinoma (HCC) tumor tissues and promotes angiogenesis. Here, we further investigated the role of VASH2 in HCC tumor progression.

Results: Bioinformatics analyses and luciferase reporter gene assays confirmed the post-transcriptional regulation of VASH2 by miR-200a/b/c. We then used HepG2 and Hep3B cells, two representative hepatic cancer cell lines, to examine the role of VASH2 in tumors. VASH2 knockdown in HepG2 cells inhibited epithelial-mesenchymal transition (EMT), but VASH2 overexpression in Hep3B cells promoted EMT. Western blot analyses showed that VASH2 promoted EMT through the ZEB1/2 pathway.

Conclusion: VASH2 promoted invasion, reduced apoptosis and increased the proportion of stem cells in vitro and in vivo. These results indicated that VASH2 expression in HCC cells promotes the malignant transformation of tumors by inducing EMT.

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The orthotopic HCC xenograft model of HepG2 group (A) and Hep3B group (B).
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Fig7: The orthotopic HCC xenograft model of HepG2 group (A) and Hep3B group (B).

Mentions: We also built the orthotopic HCC xenograft model. As the result of the Figure 7, we could see that VASH2 overexpression promoted the tumor growth in vivo. In the contrary, VASH2 knockdown orthotopic reduced the tumor size in vivo. We also measured the orthotopic tumor volume. The result showed HepG2-shVASH2 group vs HepG2-shcont was (18.39 ± 7.87) mm3 vs (74.25 ± 24.33) mm3, while Hep3B-VASH2 group vs Hep3B group was (20.61 ± 9.98) mm3 vs (9.66 ± 2.41) mm3. The difference was statistically significant (p < 0.05).Figure 7


MiR200-upregulated Vasohibin 2 promotes the malignant transformation of tumors by inducing epithelial-mesenchymal transition in hepatocellular carcinoma.

Xue X, Zhang Y, Zhi Q, Tu M, Xu Y, Sun J, Wei J, Lu Z, Miao Y, Gao W - Cell Commun. Signal (2014)

The orthotopic HCC xenograft model of HepG2 group (A) and Hep3B group (B).
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4195883&req=5

Fig7: The orthotopic HCC xenograft model of HepG2 group (A) and Hep3B group (B).
Mentions: We also built the orthotopic HCC xenograft model. As the result of the Figure 7, we could see that VASH2 overexpression promoted the tumor growth in vivo. In the contrary, VASH2 knockdown orthotopic reduced the tumor size in vivo. We also measured the orthotopic tumor volume. The result showed HepG2-shVASH2 group vs HepG2-shcont was (18.39 ± 7.87) mm3 vs (74.25 ± 24.33) mm3, while Hep3B-VASH2 group vs Hep3B group was (20.61 ± 9.98) mm3 vs (9.66 ± 2.41) mm3. The difference was statistically significant (p < 0.05).Figure 7

Bottom Line: VASH2 knockdown in HepG2 cells inhibited epithelial-mesenchymal transition (EMT), but VASH2 overexpression in Hep3B cells promoted EMT.Western blot analyses showed that VASH2 promoted EMT through the ZEB1/2 pathway.VASH2 promoted invasion, reduced apoptosis and increased the proportion of stem cells in vitro and in vivo.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, the First Affiliated Hospital with Nanjing Medical University, 300# Guangzhou Road, Nanjing, 210029, China. xfxue@suda.edu.cn.

ABSTRACT

Background: Hepatocellular carcinoma (HCC) typically relies on tumor transformation and angiogenesis for its malignant behavior, including growth and metastasis. Previously, we reported that Vasohibin2 (VASH2) is preferentially expressed in hepatocellular carcinoma (HCC) tumor tissues and promotes angiogenesis. Here, we further investigated the role of VASH2 in HCC tumor progression.

Results: Bioinformatics analyses and luciferase reporter gene assays confirmed the post-transcriptional regulation of VASH2 by miR-200a/b/c. We then used HepG2 and Hep3B cells, two representative hepatic cancer cell lines, to examine the role of VASH2 in tumors. VASH2 knockdown in HepG2 cells inhibited epithelial-mesenchymal transition (EMT), but VASH2 overexpression in Hep3B cells promoted EMT. Western blot analyses showed that VASH2 promoted EMT through the ZEB1/2 pathway.

Conclusion: VASH2 promoted invasion, reduced apoptosis and increased the proportion of stem cells in vitro and in vivo. These results indicated that VASH2 expression in HCC cells promotes the malignant transformation of tumors by inducing EMT.

Show MeSH
Related in: MedlinePlus