Effect of Insulin-like Growth Factor-1 on Bone Morphogenetic Protein-2 Expression in Hepatic Carcinoma SMMC7721 Cells through the p38 MAPK Signaling Pathway

Objective: To observe the effect of insulin-like growth factor-1 (IGF-1) on bone morphogenetic protein(BMP)-2 expression in hepatocellular carcinoma SMMC7721 cells.
Methods: Cells were divided into blankcontrol, IGF-1, IGF-1 + SB203580, and SB203580 groups. SB203580 was used to block the p38 MAPK signalingpathway. Changes in the expression of BMP-2, p38 MAPK, and phosphorylated p38, MERK, ERK and JNKwere determined using reverse transcription polymerase chain reactions (RT-PCR) and Western blot analysis.
Results: Protein expression of phosphorylated BMP-2, MERK, ERK, and JNK was significantly up-regulatedby IGF-1 compared with the control group (1.138 ± 0.065 vs. 0.606 ± 0.013, 0.292 ± 0.005 vs. 0.150 ± 0.081,0.378 ± 0.006 vs. 0.606 ± 0.013, and 0.299 ± 0.015 vs. 0.196 ± 0.017, respectively; P < 0.05). Levels of BMP-2 andphosphorylated MERK and JNK were significantly reduced after blocking of the p38MAPK signaling pathway(0.494 ± 0.052 vs. 0.165 ± 0.017, 0.073 ± 0.07 vs. 0.150 ± 0.081, and 0.018 ± 0.008 vs. 0.196 ± 0.017, respectively; P< 0.05), but such a significant difference was not observed for phosphorylated ERK protein expression (0.173 ±0.07 vs. 0.150 ± 0.081, P > 0.05).
Conclusion: IGF-1 can up-regulate BMP-2 expression, and p38 MAPK signalingpathway blockage can noticeably reduce the up-regulated expression. We can conclude that the up-regulatoryeffect of IGF-1 on BMP-2 expression is realized through the p38 MAPK signaling pathway.