Down-regulated expressions of PPARγ and its coactivator PGC-1 are related to gastric carcinogenesis and Lauren’s classification in gastric carcinoma
Abstract
Objective: To explore the relationship between peroxisome proliferator activated receptor-gamma (PPARγ) and peroxisome proliferator-activated receptor-gamma coactivator-1 (PGC-1) expression in gastric carcinoma (GC), and analyze their correlations with clinicopathological features and clinical outcomes of patients.
Methods: The two-step immunohistochemical method was used to detect the expression of PPARγ and PGC-1 in 179 cases of GC, and 108 cases of matched normal gastric mucosa. Besides, 16 cases of fresh GC specimens and corresponding normal gastric mucosa were detected for PGC-1 expression with Western blotting.
Results: The positive rates of PPARγ and PGC-1 expression were significantly lower in GC (54.75%, 49.16%) than in normal gastric mucosa (70.37%, 71.30%), respectively (P<0.05). The decreased expression of PGC-1 in GC was confirmed in our Western blot analysis (P=0.004). PPARγ and PGC-1 expressions were related to Lauren’s types of GC (P<0.05). Positive correlation was found between PPARγ and PGC-1 expression in GC (rk=0.422, P<0.001). The survival time of PPARγ negative and positive patients was 36.6±3.0 vs. 38.5±2.7 months, and no statistical difference was found between the 5-year survival rates of two groups (34.4% vs. 44.1%, P=0.522, log-rank test); the survival time of PGC-1 negative and positive patients was 36.2±2.8 vs. 39.9±2.9 months, while no statistical difference was found between the 5-year survival rates of the two groups (32.0% vs. 48.2%, P=0.462, log-rank test)
Conclusions: Decreased expression of PPARγ and PGC-1 in GC was related to the Lauren’s classification. Their expressions in GC were positively correlated, indicating that their functions in gastric carcinogenesis may be closely related.
Methods: The two-step immunohistochemical method was used to detect the expression of PPARγ and PGC-1 in 179 cases of GC, and 108 cases of matched normal gastric mucosa. Besides, 16 cases of fresh GC specimens and corresponding normal gastric mucosa were detected for PGC-1 expression with Western blotting.
Results: The positive rates of PPARγ and PGC-1 expression were significantly lower in GC (54.75%, 49.16%) than in normal gastric mucosa (70.37%, 71.30%), respectively (P<0.05). The decreased expression of PGC-1 in GC was confirmed in our Western blot analysis (P=0.004). PPARγ and PGC-1 expressions were related to Lauren’s types of GC (P<0.05). Positive correlation was found between PPARγ and PGC-1 expression in GC (rk=0.422, P<0.001). The survival time of PPARγ negative and positive patients was 36.6±3.0 vs. 38.5±2.7 months, and no statistical difference was found between the 5-year survival rates of two groups (34.4% vs. 44.1%, P=0.522, log-rank test); the survival time of PGC-1 negative and positive patients was 36.2±2.8 vs. 39.9±2.9 months, while no statistical difference was found between the 5-year survival rates of the two groups (32.0% vs. 48.2%, P=0.462, log-rank test)
Conclusions: Decreased expression of PPARγ and PGC-1 in GC was related to the Lauren’s classification. Their expressions in GC were positively correlated, indicating that their functions in gastric carcinogenesis may be closely related.