2. Academic Validation
  3. PEG10 overexpression induced by E2F-1 promotes cell proliferation, migration, and invasion in pancreatic cancer

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.
Yun-Peng Peng 1 2,  Yi Zhu 1 2,  Ling-Di Yin 1 2,  Jing-Jing Zhang 1 2,  Ji-Shu Wei 1 2,  Xian Liu 1 2,  Xin-Chun Liu 1 2,  Wen-Tao Gao 1 2,  Kui-Rong Jiang 1 2,  Yi Miao 3 4
Affiliations

Affiliations

  • 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].
PMID: 28193232 DOI: 10.1186/s13046-017-0500-x
Abstract

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.

Keywords

E2F-1; PEG10; Pancreatic cancer; Progression.

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