TY - JOUR
T1 - Effects of PPAR-γ agonists on oral cancer cell lines
T2 - Potential horizons for chemopreventives and adjunctive therapies
AU - Hall, Jeffrey A.
AU - Rusten, Mark
AU - Abughazaleh, Raed D.
AU - Wuertz, Beverly
AU - Souksavong, Vannesa
AU - Escher, Paul
AU - Ondrey, Frank
N1 - Funding Information:
Lion's 5M Hearing Center Grant (Minnesota); National Cancer Institute/National Institute of Health, Grant/Award Number: P30 CA77598-07
Publisher Copyright:
© 2020 Wiley Periodicals, Inc.
PY - 2020/9/1
Y1 - 2020/9/1
N2 - Background: Peroxisome proliferator-activated receptor-gamma (PPAR-γ) activators have anti-cancer effects. Our objective was to determine the effect of PPAR-γ ligands 15-deoxy-D12,14-Prostaglandin J2 (15-PGJ2) and ciglitazone on proliferation, apoptosis, and NF-κB in human oral squamous cell carcinoma cell lines. Methods: NA and CA9-22 cells were treated in vitro with 15-PGJ2 and ciglitazone. Proliferation was measured by MTT colorimetric assay and cell cycle analysis performed via flow cytometry, apoptosis by caspase-3 colorimetric assay and poly-(ADP-ribose) polymerase cleavage on Western blot, and NF-κB activation by luciferase assays. Results: MTT assays demonstrated dose-dependent decreases after 15-PGJ2 treatment in both cell lines, and S-phase cell cycle arrest was also demonstrated. NF-κB luciferase reporter gene activity decreased seven- and eightfold in NA and CA9-22 cells, respectively. Caspase-3 activity increased two- and eightfold in NA and CA9-22 cells, respectively. Conclusions: Our results suggest these agents, in addition to activating PPAR-γ, can downregulate NF-κB and potentiate apoptosis in oral cancer cells.
AB - Background: Peroxisome proliferator-activated receptor-gamma (PPAR-γ) activators have anti-cancer effects. Our objective was to determine the effect of PPAR-γ ligands 15-deoxy-D12,14-Prostaglandin J2 (15-PGJ2) and ciglitazone on proliferation, apoptosis, and NF-κB in human oral squamous cell carcinoma cell lines. Methods: NA and CA9-22 cells were treated in vitro with 15-PGJ2 and ciglitazone. Proliferation was measured by MTT colorimetric assay and cell cycle analysis performed via flow cytometry, apoptosis by caspase-3 colorimetric assay and poly-(ADP-ribose) polymerase cleavage on Western blot, and NF-κB activation by luciferase assays. Results: MTT assays demonstrated dose-dependent decreases after 15-PGJ2 treatment in both cell lines, and S-phase cell cycle arrest was also demonstrated. NF-κB luciferase reporter gene activity decreased seven- and eightfold in NA and CA9-22 cells, respectively. Caspase-3 activity increased two- and eightfold in NA and CA9-22 cells, respectively. Conclusions: Our results suggest these agents, in addition to activating PPAR-γ, can downregulate NF-κB and potentiate apoptosis in oral cancer cells.
KW - 15-deoxy-D-prostaglandin J (15-PGJ)
KW - Ciglitazone
KW - NF-κB
KW - PPAR-γ
KW - squamous cell carcinoma
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U2 - 10.1002/hed.26286
DO - 10.1002/hed.26286
M3 - Article
C2 - 32519370
AN - SCOPUS:85086167500
SN - 1043-3074
VL - 42
SP - 2542
EP - 2554
JO - Head and Neck Surgery
JF - Head and Neck Surgery
IS - 9
ER -
