PEG10 overexpression induced by E2F-1 promotes cell proliferation, migration, and invasion in pancreatic cancer
- J Exp Clin Cancer Res. 2017 Feb 13;36(1):30. doi: 10.1186/s13046-017-0500-x.
- 1. Pancreas Center, First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029, Jiangsu Province, People's Republic of China.
- 2. Pancreas Institute, Nanjing Medical University, Nanjing, 210029, Jiangsu Province, People's Republic of China.
- 3. Pancreas Center, First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029, Jiangsu Province, People's Republic of China. [email protected].
- 4. Pancreas Institute, Nanjing Medical University, Nanjing, 210029, Jiangsu Province, People's Republic of China. [email protected].
Background: Overexpression of paternally expressed gene-10 (PEG10) is known to promote the progression of several carcinomas, however, its role in pancreatic Cancer (PC) is unknown. We investigated the expression and function of PEG10 in PC.
Methods: PEG10 expression and correlation with PC progression was assessed in cancerous tissues and paired non-cancerous tissues. Further, the role of PEG10 in PC cell progression and the underlying mechanisms were studied by using small interfering RNA (Si-RNA).
Results: PEG10 expression was significantly higher in cancerous tissues and correlated with PC invasion of vessels and Ki-67 expression. Si-RNA mediated PEG10 knockdown resulted in inhibition of proliferation and G0/G1 cell cycle arrest, which was mediated by p21 and p27 upregulation. A decrease in PC cell invasion and migration, mediated by ERK/MMP7 pathway, was observed in PEG10 knockdown group. Further, findings of ChIP assay suggested that E2F-1 could directly enhance the expression of PEG10 through binding to PEG10 promoter.
Conclusions: In conclusion, PEG10 was identified as a prognostic biomarker for PC and E2F-1 induced PEG10 could promote PC cell proliferation, invasion, and metastasis.