PEBP4 promoted the growth and migration of cancer cells in pancreatic ductal adenocarcinoma

被引:13
|
作者
Zhang, Dexiang [1 ]
Dai, Yuedi [2 ]
Cai, Yuankun [1 ]
Suo, Tao [3 ]
Liu, Han [3 ]
Wang, Yueqi [3 ]
Cheng, Zhijian [1 ]
Liu, Houbao [3 ]
机构
[1] Fudan Univ, Peoples Hosp Shanghai 5, Dept Gen Surg, 128 Ruili Rd, Shanghai 200240, Peoples R China
[2] Fudan Univ, Minhang Branch, Dept Med Oncol, Canc Hosp, Shanghai 200240, Peoples R China
[3] Fudan Univ, Gen Surg Inst, Zhongshan Hosp, Dept Gen Surg, 180 Fenglin Rd, Shanghai 200032, Peoples R China
基金
中国国家自然科学基金;
关键词
PEBP4; PDAC; AKT; Cell growth and migration; PROTEIN RKIP; PATHWAY; TARGET; EXPRESSION; MTOR;
D O I
10.1007/s13277-015-3906-0
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Pancreatic ductal adenocarcinoma (PDAC) is one of the most common malignancies in the world. Numerous studies have linked the activation of AKT to the progression of PDAC. Phosphatidylethanolamine-binding protein 4 (PEBP4) has been reported to be upregulated in various cancer types. However, its expression pattern and biological functions in PDAC are unknown. In this study, it was found that the messenger RNA (mRNA) and protein level of PEBP4 was elevated in PDAC samples. Forced expression of PEBP4 in PDAC cell lines promoted cell growth and migration, while downregulation of PEBP4 in PDAC cells by RNA interference (RNAi) inhibited the growth, migration, and metastasis of the cancer cells. PEBP4 interacted with AKT and promoted the phosphorylation of serine 473 in AKT. Collectively, this study suggested that PEBP4 might promote the progression of PDAC through activating AKT signaling and PEBP4 might be a promising therapeutic target for PDAC treatment.
引用
收藏
页码:1699 / 1705
页数:7
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