Limits...
Overexpression of candidate tumor suppressor ECRG4 inhibits glioma proliferation and invasion.

Li W, Liu X, Zhang B, Qi D, Zhang L, Jin Y, Yang H - J. Exp. Clin. Cancer Res. (2010)

Bottom Line: Cells transfected with ECRG4 showed significantly decreased cell proliferation as evaluated by MTT and colony formation assays.Furthermore, overexpression inhibited cell migration and invasion in transwell and Boyden chamber experiments and retarded the cell cycle progression from G1 to S phase by FACSCaliber cytometry.Protein levels of nuclear transcription factor NF-kB, which is involved in cell proliferation, inversely correlated with ECRG4 expression.

View Article: PubMed Central - HTML - PubMed

Affiliation: The Key Laboratory of Pathobiology, Ministry of Education, Jilin University, 130021, PR China.

ABSTRACT

Background: ECRG4 has been shown to be a candidate tumor suppressor in several tumors, but its role in glioma remains poorly understood. In this study, we examined the mRNA expression of ECRG4 and investigated its biological role in glioma cells.

Methods: Real-time PCR was used to examine expression of ECRG4 in gliomas and their matched brain tissues. The effect of ECRG4 expression on cell proliferation, invasion, and migration was investigated in human U251 glioma cells. Finally, the regulation of transcription factor NF-kB by ECRG4 was evaluated by western blotting.

Results: Of the 10 paired samples analyzed, 9 glioma tissues displayed the decreased expression of ECRG4 compared to matched normal brain tissues. Cells transfected with ECRG4 showed significantly decreased cell proliferation as evaluated by MTT and colony formation assays. Furthermore, overexpression inhibited cell migration and invasion in transwell and Boyden chamber experiments and retarded the cell cycle progression from G1 to S phase by FACSCaliber cytometry. Protein levels of nuclear transcription factor NF-kB, which is involved in cell proliferation, inversely correlated with ECRG4 expression.

Conclusion: Our data suggest that ECRG4 serves as a tumor suppressor in glioma.

Show MeSH

Related in: MedlinePlus

Increased ECRG4 expression inhibited cell migration, invasion and cell cycle progression. (A) Cell migration and (B)invasion capabilities of Control-vector cells, pEGFP-ECRG4-5 and -7 cells, were examined using transwell assay and boyden chamber assay. Data were presented as mean ± SD for three independent experiments. *P < 0.05, as compared to Control-vector cells. C. Cell cycle in parental U251 cells, Control-vector cells and pEGFP-ECRG4-5 and -7 cells, was determined by FACS Caliber cytometry. *P < 0.05, as compared to parental U251 cells and Control-vector cells
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC2913949&req=5

Figure 4: Increased ECRG4 expression inhibited cell migration, invasion and cell cycle progression. (A) Cell migration and (B)invasion capabilities of Control-vector cells, pEGFP-ECRG4-5 and -7 cells, were examined using transwell assay and boyden chamber assay. Data were presented as mean ± SD for three independent experiments. *P < 0.05, as compared to Control-vector cells. C. Cell cycle in parental U251 cells, Control-vector cells and pEGFP-ECRG4-5 and -7 cells, was determined by FACS Caliber cytometry. *P < 0.05, as compared to parental U251 cells and Control-vector cells

Mentions: To measure the effect of ECRG4 on cell migration, ECRG4-expressing ECRG4-5 and -7 cells were cultured on a transwell apparatus. After 12-h incubation, cell migration was significantly decreased in both ECRG4-overexpressed cell groups compared to the parental U251 cells and the ECRG4-negative control cells (for both P < 0.001) (Figure 4A). Using a Boyden chamber coated with matrigel, we measured cell invasion after 16-h incubation. Compared with the negative control cells, ECRG4-expressing -5 and -7 cells both showed significantly decreased invasiveness (for both P < 0.001) (Fig 4.B).


Overexpression of candidate tumor suppressor ECRG4 inhibits glioma proliferation and invasion.

Li W, Liu X, Zhang B, Qi D, Zhang L, Jin Y, Yang H - J. Exp. Clin. Cancer Res. (2010)

Increased ECRG4 expression inhibited cell migration, invasion and cell cycle progression. (A) Cell migration and (B)invasion capabilities of Control-vector cells, pEGFP-ECRG4-5 and -7 cells, were examined using transwell assay and boyden chamber assay. Data were presented as mean ± SD for three independent experiments. *P < 0.05, as compared to Control-vector cells. C. Cell cycle in parental U251 cells, Control-vector cells and pEGFP-ECRG4-5 and -7 cells, was determined by FACS Caliber cytometry. *P < 0.05, as compared to parental U251 cells and Control-vector cells
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2913949&req=5

Figure 4: Increased ECRG4 expression inhibited cell migration, invasion and cell cycle progression. (A) Cell migration and (B)invasion capabilities of Control-vector cells, pEGFP-ECRG4-5 and -7 cells, were examined using transwell assay and boyden chamber assay. Data were presented as mean ± SD for three independent experiments. *P < 0.05, as compared to Control-vector cells. C. Cell cycle in parental U251 cells, Control-vector cells and pEGFP-ECRG4-5 and -7 cells, was determined by FACS Caliber cytometry. *P < 0.05, as compared to parental U251 cells and Control-vector cells
Mentions: To measure the effect of ECRG4 on cell migration, ECRG4-expressing ECRG4-5 and -7 cells were cultured on a transwell apparatus. After 12-h incubation, cell migration was significantly decreased in both ECRG4-overexpressed cell groups compared to the parental U251 cells and the ECRG4-negative control cells (for both P < 0.001) (Figure 4A). Using a Boyden chamber coated with matrigel, we measured cell invasion after 16-h incubation. Compared with the negative control cells, ECRG4-expressing -5 and -7 cells both showed significantly decreased invasiveness (for both P < 0.001) (Fig 4.B).

Bottom Line: Cells transfected with ECRG4 showed significantly decreased cell proliferation as evaluated by MTT and colony formation assays.Furthermore, overexpression inhibited cell migration and invasion in transwell and Boyden chamber experiments and retarded the cell cycle progression from G1 to S phase by FACSCaliber cytometry.Protein levels of nuclear transcription factor NF-kB, which is involved in cell proliferation, inversely correlated with ECRG4 expression.

View Article: PubMed Central - HTML - PubMed

Affiliation: The Key Laboratory of Pathobiology, Ministry of Education, Jilin University, 130021, PR China.

ABSTRACT

Background: ECRG4 has been shown to be a candidate tumor suppressor in several tumors, but its role in glioma remains poorly understood. In this study, we examined the mRNA expression of ECRG4 and investigated its biological role in glioma cells.

Methods: Real-time PCR was used to examine expression of ECRG4 in gliomas and their matched brain tissues. The effect of ECRG4 expression on cell proliferation, invasion, and migration was investigated in human U251 glioma cells. Finally, the regulation of transcription factor NF-kB by ECRG4 was evaluated by western blotting.

Results: Of the 10 paired samples analyzed, 9 glioma tissues displayed the decreased expression of ECRG4 compared to matched normal brain tissues. Cells transfected with ECRG4 showed significantly decreased cell proliferation as evaluated by MTT and colony formation assays. Furthermore, overexpression inhibited cell migration and invasion in transwell and Boyden chamber experiments and retarded the cell cycle progression from G1 to S phase by FACSCaliber cytometry. Protein levels of nuclear transcription factor NF-kB, which is involved in cell proliferation, inversely correlated with ECRG4 expression.

Conclusion: Our data suggest that ECRG4 serves as a tumor suppressor in glioma.

Show MeSH
Related in: MedlinePlus