Abstract
The Wnt/β-catenin signaling pathway plays a key role during hepatocellular carcinoma (HCC) genesis and development. The present study aimed to investigate the effects of the Wnt/β-catenin signaling pathway on the expression of angiogenic growth factors involved in HCC. The HCC HepG2 cell line was transfected with small interfering RNA (siRNA) against β-catenin. After 72 and 96 h, protein was extracted and the expression levels of β-catenin, matrix metalloproteinase (MMP)-2, MMP-9, vascular endothelial growth factor (VEGF)-A, VEGF-C and basic fibroblast growth factor (bFGF) were detected by western blot analysis. β-catenin protein expression was inhibited at both time points. Notably, MMP-2, MMP-9, VEGF-A, VEGF-C and bFGF protein expression levels decreased at 72 h and then increased at 96 h after transfection. Our results demonstrated that in HCC cells, the Wnt/β-catenin signaling pathway may regulate the protein expression of the angiogenic factors, MMP-2, MMP-9, VEGF-A, VEGF-C and bFGF. These proteins were downstream of β-catenin signaling and were also regulated by other factors. In conclusion, the Wnt/β-catenin signaling pathway may contribute to the regulation of HCC angiogenesis, infiltration and metastasis through regulating the expression of these angiogenic factors.
Highlights
The cytoplasmic protein, β‐catenin, is a central molecule in the Wnt signaling pathway and plays a key role in the genesis and development of tumors
matrix metalloproteinase (MMP)‐2 and ‐9 protein expression was inhibited at 72 h, but that of MMP‐2 had returned to normal levels after 96 h (t=0.68; P>0.05)
MMP‐9 expression levels were increased at 96 h, but were less than the levels observed in the control group (t=19.74; P
Summary
The cytoplasmic protein, β‐catenin, is a central molecule in the Wnt signaling pathway and plays a key role in the genesis and development of tumors. When β‐catenin phosphorylation and ubiquitin‐dependent degradation are inhibited, β‐catenin concentrates in the cytoplasm and forms a complex with the transcription factor, lymphoid enhancing factor‐1 (LEF1)̸T‐cell factor (TCF), which is subsequently transported into cell nuclei. This transcription complex activates the expression of downstream target genes, resulting in abnormal cell proliferation and cell carcinogenesis [6]. Further research on the target genes of the Wntβ‐catenin signaling pathway is required to increase our understanding of the role of this pathway in the genesis and development of tumors
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