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15-PGJ2, but not thiazolidinediones, inhibits cell growth, induces apoptosis, and causes downregulation of Stat3 in human oral SCCa cells.

Nikitakis NG, Siavash H, Hebert C, Reynolds MA, Hamburger AW, Sauk JJ - Br. J. Cancer (2002)

Bottom Line: Interestingly, rosiglitazone and ciglitazone, two members of the thiazolidinedione family of PPARgamma activators, did not exert a growth inhibitory effect.In contrast, other PPARgamma did not induce similar effects.Our results provide the first evidence of significant antineoplastic effects of 15-PGJ(2) on human oral squamous cell carcinoma cells, which may be related to downmodulation of Stat3 and are at least partly mediated through PPARgamma-independent events.

View Article: PubMed Central - PubMed

Affiliation: Department of Diagnostic Sciences and Pathology, University of Maryland, 666 W. Baltimore Street, Room 4-C-02, Baltimore, MD 21201, USA. nin001@dental.umaryland.edu

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Effect of 15-deoxy-Δ12,14-PGJ2 on levels of apoptosis of oral SCC25 and SCC9 cells treated with 0.1% DMSO or 20 μM of the drug for 72 h. Treatment with 15-deoxy-Δ12,14-PGJ2 resulted in a statistically significant increase in apoptosis compared to DMSO-treated control cells. Similar results were obtained from the other oral SCCa cell lines tested.
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fig3: Effect of 15-deoxy-Δ12,14-PGJ2 on levels of apoptosis of oral SCC25 and SCC9 cells treated with 0.1% DMSO or 20 μM of the drug for 72 h. Treatment with 15-deoxy-Δ12,14-PGJ2 resulted in a statistically significant increase in apoptosis compared to DMSO-treated control cells. Similar results were obtained from the other oral SCCa cell lines tested.

Mentions: Treatment of oral SCCa cells with 10 or 20 μM of 15-PGJ2 did not significantly affect the percentage of cells in the S phase of the cell cycle, which remained stable or was only slightly increased; however, an increase in the percentage of cells in the G2 phase of the cell cycle was observed, accompanied by a corresponding reduction of cells in the G1 phase (Table 2Table 2Cell cycle profiles of oral SCC25 and SCC9 cells treated with 20 μM of 15-PGJ2 or the vehicle alone (0.1% DMSO)). These results indicate a relative accumulation of cells in the G2 phase, which may interfere with cell cycle progression. On the other hand, significant 5–8-fold increases in the levels of apoptosis resulted following treatment with 15-deoxy-Δ12,14-PGJ2 for 72 h at concentrations ranging from 10 to 20 μM (F2,4=9.5, P⩽0.05) (Figure 3Figure 3


15-PGJ2, but not thiazolidinediones, inhibits cell growth, induces apoptosis, and causes downregulation of Stat3 in human oral SCCa cells.

Nikitakis NG, Siavash H, Hebert C, Reynolds MA, Hamburger AW, Sauk JJ - Br. J. Cancer (2002)

Effect of 15-deoxy-Δ12,14-PGJ2 on levels of apoptosis of oral SCC25 and SCC9 cells treated with 0.1% DMSO or 20 μM of the drug for 72 h. Treatment with 15-deoxy-Δ12,14-PGJ2 resulted in a statistically significant increase in apoptosis compared to DMSO-treated control cells. Similar results were obtained from the other oral SCCa cell lines tested.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2376283&req=5

fig3: Effect of 15-deoxy-Δ12,14-PGJ2 on levels of apoptosis of oral SCC25 and SCC9 cells treated with 0.1% DMSO or 20 μM of the drug for 72 h. Treatment with 15-deoxy-Δ12,14-PGJ2 resulted in a statistically significant increase in apoptosis compared to DMSO-treated control cells. Similar results were obtained from the other oral SCCa cell lines tested.
Mentions: Treatment of oral SCCa cells with 10 or 20 μM of 15-PGJ2 did not significantly affect the percentage of cells in the S phase of the cell cycle, which remained stable or was only slightly increased; however, an increase in the percentage of cells in the G2 phase of the cell cycle was observed, accompanied by a corresponding reduction of cells in the G1 phase (Table 2Table 2Cell cycle profiles of oral SCC25 and SCC9 cells treated with 20 μM of 15-PGJ2 or the vehicle alone (0.1% DMSO)). These results indicate a relative accumulation of cells in the G2 phase, which may interfere with cell cycle progression. On the other hand, significant 5–8-fold increases in the levels of apoptosis resulted following treatment with 15-deoxy-Δ12,14-PGJ2 for 72 h at concentrations ranging from 10 to 20 μM (F2,4=9.5, P⩽0.05) (Figure 3Figure 3

Bottom Line: Interestingly, rosiglitazone and ciglitazone, two members of the thiazolidinedione family of PPARgamma activators, did not exert a growth inhibitory effect.In contrast, other PPARgamma did not induce similar effects.Our results provide the first evidence of significant antineoplastic effects of 15-PGJ(2) on human oral squamous cell carcinoma cells, which may be related to downmodulation of Stat3 and are at least partly mediated through PPARgamma-independent events.

View Article: PubMed Central - PubMed

Affiliation: Department of Diagnostic Sciences and Pathology, University of Maryland, 666 W. Baltimore Street, Room 4-C-02, Baltimore, MD 21201, USA. nin001@dental.umaryland.edu

Show MeSH
Related in: MedlinePlus