Limits...
Peroxisome proliferator-activated receptor γ agonist efatutazone impairs transforming growth factor β2-induced motility of epidermal growth factor receptor tyrosine kinase inhibitor-resistant lung cancer cells.

Serizawa M, Murakami H, Watanabe M, Takahashi T, Yamamoto N, Koh Y - Cancer Sci. (2014)

Bottom Line: Efatutazone, a novel peroxisome proliferator-activated receptor gamma (PPARγ) agonist, is currently under clinical evaluation; it has antiproliferative effects and induces cellular morphological changes and differentiation.Efatutazone had no growth-inhibitory effect on the tested cells but inhibited the motility of EGFR-TKI-resistant cells in wound closure and transwell assays.Efatutazone plus erlotinib treatment provided greater inhibition of PC-9ER cell migration than efatutazone or erlotinib alone.

View Article: PubMed Central - PubMed

Affiliation: Drug Discovery and Development Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.

Show MeSH

Related in: MedlinePlus

Effect of efatutazone on peroxisome proliferator-activated receptor gamma (PPARγ)-mediated transcriptional activity. After the cells were transfected with the PPARγ-dependent luciferase reporter pPG2-aP2-TK, they were incubated for 24 or 48 h in FBS-free medium with DMSO (0.1%; control) or efatutazone (10 μmol/L). PPARγ-mediated transcriptional activity was measured with a luciferase reporter assay as described in the Materials and Methods. The values were normalized relative to the Renilla luciferase activity in cells cotransfected with pRL-CMV.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4317891&req=5

fig04: Effect of efatutazone on peroxisome proliferator-activated receptor gamma (PPARγ)-mediated transcriptional activity. After the cells were transfected with the PPARγ-dependent luciferase reporter pPG2-aP2-TK, they were incubated for 24 or 48 h in FBS-free medium with DMSO (0.1%; control) or efatutazone (10 μmol/L). PPARγ-mediated transcriptional activity was measured with a luciferase reporter assay as described in the Materials and Methods. The values were normalized relative to the Renilla luciferase activity in cells cotransfected with pRL-CMV.

Mentions: Efatutazone treatment induced PPARγ-mediated transcriptional activity in PC-9 and PC-9ZD cells, but not in PC-9ER cells (Fig. 4), suggesting that the inhibitory effect of efatutazone on the motility of PC-9ER cells may not be due to direct activation of PPARγ signaling, but rather may be due to off-target effects.


Peroxisome proliferator-activated receptor γ agonist efatutazone impairs transforming growth factor β2-induced motility of epidermal growth factor receptor tyrosine kinase inhibitor-resistant lung cancer cells.

Serizawa M, Murakami H, Watanabe M, Takahashi T, Yamamoto N, Koh Y - Cancer Sci. (2014)

Effect of efatutazone on peroxisome proliferator-activated receptor gamma (PPARγ)-mediated transcriptional activity. After the cells were transfected with the PPARγ-dependent luciferase reporter pPG2-aP2-TK, they were incubated for 24 or 48 h in FBS-free medium with DMSO (0.1%; control) or efatutazone (10 μmol/L). PPARγ-mediated transcriptional activity was measured with a luciferase reporter assay as described in the Materials and Methods. The values were normalized relative to the Renilla luciferase activity in cells cotransfected with pRL-CMV.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4317891&req=5

fig04: Effect of efatutazone on peroxisome proliferator-activated receptor gamma (PPARγ)-mediated transcriptional activity. After the cells were transfected with the PPARγ-dependent luciferase reporter pPG2-aP2-TK, they were incubated for 24 or 48 h in FBS-free medium with DMSO (0.1%; control) or efatutazone (10 μmol/L). PPARγ-mediated transcriptional activity was measured with a luciferase reporter assay as described in the Materials and Methods. The values were normalized relative to the Renilla luciferase activity in cells cotransfected with pRL-CMV.
Mentions: Efatutazone treatment induced PPARγ-mediated transcriptional activity in PC-9 and PC-9ZD cells, but not in PC-9ER cells (Fig. 4), suggesting that the inhibitory effect of efatutazone on the motility of PC-9ER cells may not be due to direct activation of PPARγ signaling, but rather may be due to off-target effects.

Bottom Line: Efatutazone, a novel peroxisome proliferator-activated receptor gamma (PPARγ) agonist, is currently under clinical evaluation; it has antiproliferative effects and induces cellular morphological changes and differentiation.Efatutazone had no growth-inhibitory effect on the tested cells but inhibited the motility of EGFR-TKI-resistant cells in wound closure and transwell assays.Efatutazone plus erlotinib treatment provided greater inhibition of PC-9ER cell migration than efatutazone or erlotinib alone.

View Article: PubMed Central - PubMed

Affiliation: Drug Discovery and Development Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.

Show MeSH
Related in: MedlinePlus