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MED30 Regulates the Proliferation and Motility of Gastric Cancer Cells.

Lee YJ, Han ME, Baek SJ, Kim SY, Oh SO - PLoS ONE (2015)

Bottom Line: It was found that MED30 was overexpressed in gastric cancer tissues and cell lines.Moreover, MED30 overexpression increased the proliferation, migration, and invasion of gastric cancer cells, whereas MED30 knockdown inhibited these effects.MED30 also promoted the expressions of genes related to epithelial-mesenchymal transition and induced a fibroblast-like morphology.

View Article: PubMed Central - PubMed

Affiliation: Department of Anatomy, School of Medicine, Pusan National University, Busan, Republic of Korea.

ABSTRACT
MED30 is an essential member of the mediator complex that forms a hub between transcriptional activators and RNA polymerase II. However, the expressions and roles of MED30 have been poorly characterized in cancer. In this study, we examined the functional roles of MED30 during gastric cancer progression. It was found that MED30 was overexpressed in gastric cancer tissues and cell lines. Moreover, MED30 overexpression increased the proliferation, migration, and invasion of gastric cancer cells, whereas MED30 knockdown inhibited these effects. Furthermore the knockdown significantly inhibited tumorigenicity in SCID mice. MED30 also promoted the expressions of genes related to epithelial-mesenchymal transition and induced a fibroblast-like morphology. This study shows MED30 has pathophysiological roles in the proliferation, migration, and invasion of gastric cancer cells and suggests that MED30 should be viewed as a potent therapeutic target for malignant gastric carcinoma.

No MeSH data available.


Related in: MedlinePlus

MED30 induced the invasion of gastric cancer cells.Cell invasion was examined using a Matrigel invasion assay. (A) Knockdown of MED30 significantly inhibited the FBS-induced invasions of SNU216 and SNU638 cells as compared with SCR siRNA. (B) MED30 overexpression (MED30-over) enhanced cell invasion compared with the mock control. (C) Invaded cells were counted and results are presented as a bar graph. Values are the means ± SDs of three independent experiments performed in triplicate. *, p< 0.01 (Student’s t test, versus SCR or Mock). Bar; 100 μm.
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pone.0130826.g004: MED30 induced the invasion of gastric cancer cells.Cell invasion was examined using a Matrigel invasion assay. (A) Knockdown of MED30 significantly inhibited the FBS-induced invasions of SNU216 and SNU638 cells as compared with SCR siRNA. (B) MED30 overexpression (MED30-over) enhanced cell invasion compared with the mock control. (C) Invaded cells were counted and results are presented as a bar graph. Values are the means ± SDs of three independent experiments performed in triplicate. *, p< 0.01 (Student’s t test, versus SCR or Mock). Bar; 100 μm.

Mentions: To determine the role played by MED30 in the migration of gastric cancer cells, we used a Boyden chamber assay. Knockdown of MED30 decreased FBS-induced migrations of SNU216 and SNU638 cells by 90% and 52%, respectively, versus SCR transfected cells (Fig 3A and 3C). Moreover, MED30 overexpression increased the FBS-induced migration of SNU216 and SNU638 cells by 3.2 and 2.8 fold, respectively, versus mock cells (Fig 3B and 3C). These results led us to examine the role of MED30 in the invasion of gastric cancer cells. In a Matrigel invasion assay, MED30 siRNA inhibited FBS-induced invasions of SNU216 and SNU638 cells versus SCR siRNA by 64% and 47%, respectively (Fig 4A and 4C), and MED30 overexpression accelerated the FBS-induced invasions of SNU216 and SNU638 cells versus mock cells by 2.5 and 2.2 fold, respectively (Fig 4B and 4C).


MED30 Regulates the Proliferation and Motility of Gastric Cancer Cells.

Lee YJ, Han ME, Baek SJ, Kim SY, Oh SO - PLoS ONE (2015)

MED30 induced the invasion of gastric cancer cells.Cell invasion was examined using a Matrigel invasion assay. (A) Knockdown of MED30 significantly inhibited the FBS-induced invasions of SNU216 and SNU638 cells as compared with SCR siRNA. (B) MED30 overexpression (MED30-over) enhanced cell invasion compared with the mock control. (C) Invaded cells were counted and results are presented as a bar graph. Values are the means ± SDs of three independent experiments performed in triplicate. *, p< 0.01 (Student’s t test, versus SCR or Mock). Bar; 100 μm.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4482445&req=5

pone.0130826.g004: MED30 induced the invasion of gastric cancer cells.Cell invasion was examined using a Matrigel invasion assay. (A) Knockdown of MED30 significantly inhibited the FBS-induced invasions of SNU216 and SNU638 cells as compared with SCR siRNA. (B) MED30 overexpression (MED30-over) enhanced cell invasion compared with the mock control. (C) Invaded cells were counted and results are presented as a bar graph. Values are the means ± SDs of three independent experiments performed in triplicate. *, p< 0.01 (Student’s t test, versus SCR or Mock). Bar; 100 μm.
Mentions: To determine the role played by MED30 in the migration of gastric cancer cells, we used a Boyden chamber assay. Knockdown of MED30 decreased FBS-induced migrations of SNU216 and SNU638 cells by 90% and 52%, respectively, versus SCR transfected cells (Fig 3A and 3C). Moreover, MED30 overexpression increased the FBS-induced migration of SNU216 and SNU638 cells by 3.2 and 2.8 fold, respectively, versus mock cells (Fig 3B and 3C). These results led us to examine the role of MED30 in the invasion of gastric cancer cells. In a Matrigel invasion assay, MED30 siRNA inhibited FBS-induced invasions of SNU216 and SNU638 cells versus SCR siRNA by 64% and 47%, respectively (Fig 4A and 4C), and MED30 overexpression accelerated the FBS-induced invasions of SNU216 and SNU638 cells versus mock cells by 2.5 and 2.2 fold, respectively (Fig 4B and 4C).

Bottom Line: It was found that MED30 was overexpressed in gastric cancer tissues and cell lines.Moreover, MED30 overexpression increased the proliferation, migration, and invasion of gastric cancer cells, whereas MED30 knockdown inhibited these effects.MED30 also promoted the expressions of genes related to epithelial-mesenchymal transition and induced a fibroblast-like morphology.

View Article: PubMed Central - PubMed

Affiliation: Department of Anatomy, School of Medicine, Pusan National University, Busan, Republic of Korea.

ABSTRACT
MED30 is an essential member of the mediator complex that forms a hub between transcriptional activators and RNA polymerase II. However, the expressions and roles of MED30 have been poorly characterized in cancer. In this study, we examined the functional roles of MED30 during gastric cancer progression. It was found that MED30 was overexpressed in gastric cancer tissues and cell lines. Moreover, MED30 overexpression increased the proliferation, migration, and invasion of gastric cancer cells, whereas MED30 knockdown inhibited these effects. Furthermore the knockdown significantly inhibited tumorigenicity in SCID mice. MED30 also promoted the expressions of genes related to epithelial-mesenchymal transition and induced a fibroblast-like morphology. This study shows MED30 has pathophysiological roles in the proliferation, migration, and invasion of gastric cancer cells and suggests that MED30 should be viewed as a potent therapeutic target for malignant gastric carcinoma.

No MeSH data available.


Related in: MedlinePlus