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Novel regulatory program for norepinephrine-induced epithelial-mesenchymal transition in gastric adenocarcinoma cell lines.

Shan T, Cui X, Li W, Lin W, Li Y, Chen X, Wu T - Cancer Sci. (2014)

Bottom Line: In this study, we show that NE does not only obviously induce EMT alterations in the morphological characteristics of gastric adenocarcinoma cells, but also increases the markers of EMT, including vimentin expression, and decreases E-cadherin expression, further resulting in cell motility and invasiveness.We also reveal that these actions are mainly mediated through the activation of β2 -AR-HIF-1α-Snail signaling pathways.In summary, this study implies that NE induces EMT in gastric adenocarcinoma through the regulation of β2 -AR-HIF-1α-Snail activity.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, Second Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, China.

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Cell invasion assay in BGC-823 gastric adenocarcinoma cells. Norepinephrine (NE) significantly (P < 0.05) stimulated cell invasion, an effect completely blocked by ICI 118551 or β2-adrenergic receptor (β2-AR) siRNA. The photograph shows the bottom side of the filter inserts with cells that have migrated through the filter pores. Columns in the graph represent the count analysis. Con, control; I, ICI 118551.
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fig08: Cell invasion assay in BGC-823 gastric adenocarcinoma cells. Norepinephrine (NE) significantly (P < 0.05) stimulated cell invasion, an effect completely blocked by ICI 118551 or β2-adrenergic receptor (β2-AR) siRNA. The photograph shows the bottom side of the filter inserts with cells that have migrated through the filter pores. Columns in the graph represent the count analysis. Con, control; I, ICI 118551.

Mentions: Epithelial–mesenchymal transition is associated with enhanced cellular progression. Our observation that NE induced EMT prompted us to examine whether NE affects the invasion of gastric adenocarcinoma cells. The motile phenotype of NE-treated cells was evaluated by invasion assay. The number of invasive cells treated with NE significantly increased compared with that in the control group. After treatment in the β2-AR siRNA-transfected cells group, the results showed that NE did not increase the number of invaded cancer cells (Fig. 8a,b); however, it accompanied changes in E-cadherin and vimentin expression (Fig. 8c,d). These results suggested that β2-AR mediates the stimulative invasion of NE in gastric adenocarcinoma cells.


Novel regulatory program for norepinephrine-induced epithelial-mesenchymal transition in gastric adenocarcinoma cell lines.

Shan T, Cui X, Li W, Lin W, Li Y, Chen X, Wu T - Cancer Sci. (2014)

Cell invasion assay in BGC-823 gastric adenocarcinoma cells. Norepinephrine (NE) significantly (P < 0.05) stimulated cell invasion, an effect completely blocked by ICI 118551 or β2-adrenergic receptor (β2-AR) siRNA. The photograph shows the bottom side of the filter inserts with cells that have migrated through the filter pores. Columns in the graph represent the count analysis. Con, control; I, ICI 118551.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4317918&req=5

fig08: Cell invasion assay in BGC-823 gastric adenocarcinoma cells. Norepinephrine (NE) significantly (P < 0.05) stimulated cell invasion, an effect completely blocked by ICI 118551 or β2-adrenergic receptor (β2-AR) siRNA. The photograph shows the bottom side of the filter inserts with cells that have migrated through the filter pores. Columns in the graph represent the count analysis. Con, control; I, ICI 118551.
Mentions: Epithelial–mesenchymal transition is associated with enhanced cellular progression. Our observation that NE induced EMT prompted us to examine whether NE affects the invasion of gastric adenocarcinoma cells. The motile phenotype of NE-treated cells was evaluated by invasion assay. The number of invasive cells treated with NE significantly increased compared with that in the control group. After treatment in the β2-AR siRNA-transfected cells group, the results showed that NE did not increase the number of invaded cancer cells (Fig. 8a,b); however, it accompanied changes in E-cadherin and vimentin expression (Fig. 8c,d). These results suggested that β2-AR mediates the stimulative invasion of NE in gastric adenocarcinoma cells.

Bottom Line: In this study, we show that NE does not only obviously induce EMT alterations in the morphological characteristics of gastric adenocarcinoma cells, but also increases the markers of EMT, including vimentin expression, and decreases E-cadherin expression, further resulting in cell motility and invasiveness.We also reveal that these actions are mainly mediated through the activation of β2 -AR-HIF-1α-Snail signaling pathways.In summary, this study implies that NE induces EMT in gastric adenocarcinoma through the regulation of β2 -AR-HIF-1α-Snail activity.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, Second Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, China.

Show MeSH
Related in: MedlinePlus