Limits...
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.

Show MeSH

Related in: MedlinePlus

Bioluminescent imaging of tumors in vivo. VASH2 interference in HepG2 cells significantly inhibited tumor growth.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Fig6: Bioluminescent imaging of tumors in vivo. VASH2 interference in HepG2 cells significantly inhibited tumor growth.

Mentions: We further investigated whether VASH2 promoted invasion in vivo. Tumor cells were injected into the tail vein of SCID mice, and the tumor cells were observed through bioluminescent imaging once a week. The final result (Figure 6) showed that VASH2 silencing significantly inhibited the invasion and metastasis of HepG2 cells. As shown in Figure 6, the HepG2-shVASH2 group presented a lower level of luminescence than the HepG2-shcont group at days 45 and 60. Similarly, VASH2 overexpression promoted the invasion and metastasis of Hep3B cells (Additional file 4: Figure S4). These results confirmed that in addition to positively regulating EMT in vitro, VASH2 promotes tumor invasion and metastasis in vivo.Figure 6


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)

Bioluminescent imaging of tumors in vivo. VASH2 interference in HepG2 cells significantly inhibited tumor growth.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Fig6: Bioluminescent imaging of tumors in vivo. VASH2 interference in HepG2 cells significantly inhibited tumor growth.
Mentions: We further investigated whether VASH2 promoted invasion in vivo. Tumor cells were injected into the tail vein of SCID mice, and the tumor cells were observed through bioluminescent imaging once a week. The final result (Figure 6) showed that VASH2 silencing significantly inhibited the invasion and metastasis of HepG2 cells. As shown in Figure 6, the HepG2-shVASH2 group presented a lower level of luminescence than the HepG2-shcont group at days 45 and 60. Similarly, VASH2 overexpression promoted the invasion and metastasis of Hep3B cells (Additional file 4: Figure S4). These results confirmed that in addition to positively regulating EMT in vitro, VASH2 promotes tumor invasion and metastasis in vivo.Figure 6

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