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Rosiglitazone Suppresses the Growth and Invasiveness of SGC-7901 Gastric Cancer Cells and Angiogenesis In Vitro via PPARgamma Dependent and Independent Mechanisms.

He Q, Pang R, Song X, Chen J, Chen H, Chen B, Hu P, Chen M - PPAR Res (2008)

Bottom Line: Although thiazolidinediones (TZDs) were found to be ligands for peroxisome proliferators-activated receptorgamma (PPARgamma), the mechanism by which TZDs exert their anticancer effect remains unclear.Moreover, rosiglitazone did not affect the expression of VEGF by SGC-7901 cells.Our results demonstrated that by PPARgamma ligand, rosiglitazone inhibited growth and invasiveness of SGC-7901 gastric cancer cells and angiogenesis in vitro via PPARgamma-dependent or -independent pathway.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, China.

ABSTRACT
Although thiazolidinediones (TZDs) were found to be ligands for peroxisome proliferators-activated receptorgamma (PPARgamma), the mechanism by which TZDs exert their anticancer effect remains unclear. Furthermore, the effect of TZDs on metastatic and angiogenesis potential of cancer cells is unknown. Our results in this paper show that rosiglitazone inhibited SGC-7901 gastric cancer cells growth, caused G1 cell cycle arrest and induced apoptosis in a dose-dependent manner. The effects of rosiglitazone on SGC-7901 cancer cells were completely reversed by treatment with PPARgamma antagonist GW9662. Rosiglitazone inhibited SGC-7901 cell migration, invasiveness, and the expression of MMP-2 in dose-dependent manner via PPARgamma-independent manner. Rosiglitazone reduced the VEGF induced angiogenesis of HUVEC in dose-dependent manner through PPARgamma-dependent pathway. Moreover, rosiglitazone did not affect the expression of VEGF by SGC-7901 cells. Our results demonstrated that by PPARgamma ligand, rosiglitazone inhibited growth and invasiveness of SGC-7901 gastric cancer cells and angiogenesis in vitro via PPARgamma-dependent or -independent pathway.

No MeSH data available.


Related in: MedlinePlus

RGZ had no effect on the secretion of VEGF of SGC-7901 cell.
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fig6: RGZ had no effect on the secretion of VEGF of SGC-7901 cell.

Mentions: To further determine whether the effect of RGZ onangiogenesis is due to the down regulation of the tumor-secreted growthfactors, we measured the expression levels of VEGF in SGC-7901 cell culturedmedium, after treatment with various concentrations of RGZ. Our resultsdemonstrated that RGZ (1–20 μM) did notchange the expression of mRNA and protein of VEGF in SGC-7901 cells (see Figures 3(a), 3(c), and Table 1), but also theresults were confirmed by ELISA (see Figure 6).


Rosiglitazone Suppresses the Growth and Invasiveness of SGC-7901 Gastric Cancer Cells and Angiogenesis In Vitro via PPARgamma Dependent and Independent Mechanisms.

He Q, Pang R, Song X, Chen J, Chen H, Chen B, Hu P, Chen M - PPAR Res (2008)

RGZ had no effect on the secretion of VEGF of SGC-7901 cell.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2542845&req=5

fig6: RGZ had no effect on the secretion of VEGF of SGC-7901 cell.
Mentions: To further determine whether the effect of RGZ onangiogenesis is due to the down regulation of the tumor-secreted growthfactors, we measured the expression levels of VEGF in SGC-7901 cell culturedmedium, after treatment with various concentrations of RGZ. Our resultsdemonstrated that RGZ (1–20 μM) did notchange the expression of mRNA and protein of VEGF in SGC-7901 cells (see Figures 3(a), 3(c), and Table 1), but also theresults were confirmed by ELISA (see Figure 6).

Bottom Line: Although thiazolidinediones (TZDs) were found to be ligands for peroxisome proliferators-activated receptorgamma (PPARgamma), the mechanism by which TZDs exert their anticancer effect remains unclear.Moreover, rosiglitazone did not affect the expression of VEGF by SGC-7901 cells.Our results demonstrated that by PPARgamma ligand, rosiglitazone inhibited growth and invasiveness of SGC-7901 gastric cancer cells and angiogenesis in vitro via PPARgamma-dependent or -independent pathway.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, China.

ABSTRACT
Although thiazolidinediones (TZDs) were found to be ligands for peroxisome proliferators-activated receptorgamma (PPARgamma), the mechanism by which TZDs exert their anticancer effect remains unclear. Furthermore, the effect of TZDs on metastatic and angiogenesis potential of cancer cells is unknown. Our results in this paper show that rosiglitazone inhibited SGC-7901 gastric cancer cells growth, caused G1 cell cycle arrest and induced apoptosis in a dose-dependent manner. The effects of rosiglitazone on SGC-7901 cancer cells were completely reversed by treatment with PPARgamma antagonist GW9662. Rosiglitazone inhibited SGC-7901 cell migration, invasiveness, and the expression of MMP-2 in dose-dependent manner via PPARgamma-independent manner. Rosiglitazone reduced the VEGF induced angiogenesis of HUVEC in dose-dependent manner through PPARgamma-dependent pathway. Moreover, rosiglitazone did not affect the expression of VEGF by SGC-7901 cells. Our results demonstrated that by PPARgamma ligand, rosiglitazone inhibited growth and invasiveness of SGC-7901 gastric cancer cells and angiogenesis in vitro via PPARgamma-dependent or -independent pathway.

No MeSH data available.


Related in: MedlinePlus