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Potassium channel ether à go-go1 is aberrantly expressed in human liposarcoma and promotes tumorigenesis.

Wu J, Zhong D, Wei Y, Wu X, Kang L, Ding Z - Biomed Res Int (2014)

Bottom Line: The ether à go-go1 (Eag1) channel is overexpressed in a variety of cancers.Then, the protein expression of Eag1 in 131 different adipose tissues from 109 patients was detected by immunohistochemistry.It was found that Eag1 was aberrantly expressed in over 67% liposarcomas, with a higher frequency than in lipoma, hyperplasia, inflammation, and normal adipose tissues.

View Article: PubMed Central - PubMed

Affiliation: Department of Orthopaedics, the Affiliated Southeast Hospital of Xiamen University, Orthopaedic Center of People's Liberation Army, Zhanghua Road 269, Zhangzhou 363000, China.

ABSTRACT
The ether à go-go1 (Eag1) channel is overexpressed in a variety of cancers. However, the expression and function of Eag1 in liposarcoma are poorly understood. In the present study, the mRNA expression of Eag1 in different adipose tissue samples was examined by real-time PCR. Then, the protein expression of Eag1 in 131 different adipose tissues from 109 patients was detected by immunohistochemistry. Next, the associations between Eag1 expression and clinicopathological features of liposarcoma were analyzed. In addition, the effects of Eag1 on liposarcoma cell proliferation and cycle were evaluated by CCK-8, colony formation, xenograft mouse model, and flow cytometry, respectively. Finally, the activation of p38 mitogen-activated protein kinase (MAPK) was detected by Western blot analysis to explain the detailed mechanisms of oncogenic potential of Eag1 in liposarcoma. It was found that Eag1 was aberrantly expressed in over 67% liposarcomas, with a higher frequency than in lipoma, hyperplasia, inflammation, and normal adipose tissues. However, Eag1 expression was not correlated with clinicopathological features of liposarcoma. Eag1 inhibitor imipramine or Eag1-shRNA significantly suppressed the proliferation of liposarcoma cells in vitro and in vivo, accompanying with accumulation of cells in the G1 phase. These results suggest that Eag1 plays an important role in regulating the proliferation and cell cycle of liposarcoma cells and might be a potential therapeutic target for liposarcoma.

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Eag1 regulates p38 MAPK activity in liposarcoma cells. Cells were infected with shRNA for 48 h. (a) Western blot analysis of phosphorylated p38 MAPK level in Ad5-Eag1-shRNA group and negative control group. (b) Densitometric analysis of the blots with GAPDH as loading control. Data are expressed as mean ± SD (n = 3). ∗∗∗P < 0.001.
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fig6: Eag1 regulates p38 MAPK activity in liposarcoma cells. Cells were infected with shRNA for 48 h. (a) Western blot analysis of phosphorylated p38 MAPK level in Ad5-Eag1-shRNA group and negative control group. (b) Densitometric analysis of the blots with GAPDH as loading control. Data are expressed as mean ± SD (n = 3). ∗∗∗P < 0.001.

Mentions: To explore the molecular mechanism underlying the oncogenic role of Eag1 in liposarcoma, we focused on p38 MAPK pathway because Eag1 has been shown to activate p38 MAPK pathway [22], which is frequently activated in a variety of tumors [23]. Western blot analysis showed that the level of phospho-p38 MAPK was lower in Ad5-Eag1-shRNA infected SW-872 and 93T449 cells than in negative control cells (Figure 6). Taken together, these data indicate that Eag1 knockdown may inhibit the activation of p38 MAPK which then promotes growth and cell cycle arrest in liposarcoma cells.


Potassium channel ether à go-go1 is aberrantly expressed in human liposarcoma and promotes tumorigenesis.

Wu J, Zhong D, Wei Y, Wu X, Kang L, Ding Z - Biomed Res Int (2014)

Eag1 regulates p38 MAPK activity in liposarcoma cells. Cells were infected with shRNA for 48 h. (a) Western blot analysis of phosphorylated p38 MAPK level in Ad5-Eag1-shRNA group and negative control group. (b) Densitometric analysis of the blots with GAPDH as loading control. Data are expressed as mean ± SD (n = 3). ∗∗∗P < 0.001.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4127296&req=5

fig6: Eag1 regulates p38 MAPK activity in liposarcoma cells. Cells were infected with shRNA for 48 h. (a) Western blot analysis of phosphorylated p38 MAPK level in Ad5-Eag1-shRNA group and negative control group. (b) Densitometric analysis of the blots with GAPDH as loading control. Data are expressed as mean ± SD (n = 3). ∗∗∗P < 0.001.
Mentions: To explore the molecular mechanism underlying the oncogenic role of Eag1 in liposarcoma, we focused on p38 MAPK pathway because Eag1 has been shown to activate p38 MAPK pathway [22], which is frequently activated in a variety of tumors [23]. Western blot analysis showed that the level of phospho-p38 MAPK was lower in Ad5-Eag1-shRNA infected SW-872 and 93T449 cells than in negative control cells (Figure 6). Taken together, these data indicate that Eag1 knockdown may inhibit the activation of p38 MAPK which then promotes growth and cell cycle arrest in liposarcoma cells.

Bottom Line: The ether à go-go1 (Eag1) channel is overexpressed in a variety of cancers.Then, the protein expression of Eag1 in 131 different adipose tissues from 109 patients was detected by immunohistochemistry.It was found that Eag1 was aberrantly expressed in over 67% liposarcomas, with a higher frequency than in lipoma, hyperplasia, inflammation, and normal adipose tissues.

View Article: PubMed Central - PubMed

Affiliation: Department of Orthopaedics, the Affiliated Southeast Hospital of Xiamen University, Orthopaedic Center of People's Liberation Army, Zhanghua Road 269, Zhangzhou 363000, China.

ABSTRACT
The ether à go-go1 (Eag1) channel is overexpressed in a variety of cancers. However, the expression and function of Eag1 in liposarcoma are poorly understood. In the present study, the mRNA expression of Eag1 in different adipose tissue samples was examined by real-time PCR. Then, the protein expression of Eag1 in 131 different adipose tissues from 109 patients was detected by immunohistochemistry. Next, the associations between Eag1 expression and clinicopathological features of liposarcoma were analyzed. In addition, the effects of Eag1 on liposarcoma cell proliferation and cycle were evaluated by CCK-8, colony formation, xenograft mouse model, and flow cytometry, respectively. Finally, the activation of p38 mitogen-activated protein kinase (MAPK) was detected by Western blot analysis to explain the detailed mechanisms of oncogenic potential of Eag1 in liposarcoma. It was found that Eag1 was aberrantly expressed in over 67% liposarcomas, with a higher frequency than in lipoma, hyperplasia, inflammation, and normal adipose tissues. However, Eag1 expression was not correlated with clinicopathological features of liposarcoma. Eag1 inhibitor imipramine or Eag1-shRNA significantly suppressed the proliferation of liposarcoma cells in vitro and in vivo, accompanying with accumulation of cells in the G1 phase. These results suggest that Eag1 plays an important role in regulating the proliferation and cell cycle of liposarcoma cells and might be a potential therapeutic target for liposarcoma.

Show MeSH
Related in: MedlinePlus