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.
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E2F-1诱导的PEG10过表达促进胰腺癌细胞增殖、迁移和侵袭
DOI：
10.1186/s13046-017-0500-x
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发表时间：
2017-02-13
期刊：
影响因子：
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通讯作者：
Miao Y
中科院分区：
文献类型：
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作者：
Peng YP;Zhu Y;Yin LD;Zhang JJ;Wei JS;Liu X;Liu XC;Gao WT;Jiang KR;Miao Y
背景父系表达基因10（PEG 10）的过表达可促进多种肿瘤的进展，但其在胰腺癌（PC）中的作用尚不清楚。方法采用免疫组化方法检测前列腺癌组织及癌旁组织中PEG 10的表达，并分析PEG 10与前列腺癌进展的关系。结果PEG 10在PC癌组织中的表达明显增高，且与PC血管浸润和Ki-67表达相关。Si-RNA介导的PEG 10敲低导致细胞增殖抑制和G 0/G1细胞周期停滞，这是由p21和p27上调介导的。PEG 10基因敲低组PC细胞的侵袭和迁移能力明显降低，这是由ERK/MMP 7信号通路介导的。结论PEG 10可作为PC的预后标志物，E2 F-1诱导的PEG 10可促进PC细胞增殖、侵袭和转移。
BackgroundOverexpression 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.MethodsPEG10 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).ResultsPEG10 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.ConclusionsIn conclusion, PEG10 was identified as a prognostic biomarker for PC and E2F-1 induced PEG10 could promote PC cell proliferation, invasion, and metastasis.