1. Academic Validation
  2. AEBP1 promotes epithelial-mesenchymal transition of gastric cancer cells by activating the NF-κB pathway and predicts poor outcome of the patients

AEBP1 promotes epithelial-mesenchymal transition of gastric cancer cells by activating the NF-κB pathway and predicts poor outcome of the patients

  • Sci Rep. 2018 Aug 10;8(1):11955. doi: 10.1038/s41598-018-29878-6.
Jun-Yan Liu 1 Lei Jiang 1 2 Jia-Jia Liu 1 Tao He 1 You-Hong Cui 3 Feng Qian 4 Pei-Wu Yu 5
Affiliations

Affiliations

  • 1 Department of General Surgery and Center of Minimal Invasive Gastrointestinal Surgery, Southwest Hospital, Third Military Medical University, Chongqing, 400038, China.
  • 2 Department of Oncology Surgery, The First Hospital of Lanzhou University, Lanzhou, 730030, China.
  • 3 Institute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Key Laboratory of Tumor Immunopathology of Ministry of Education of China, Chongqing, 400038, China.
  • 4 Department of General Surgery and Center of Minimal Invasive Gastrointestinal Surgery, Southwest Hospital, Third Military Medical University, Chongqing, 400038, China. qianfengpuwaia@163.com.
  • 5 Department of General Surgery and Center of Minimal Invasive Gastrointestinal Surgery, Southwest Hospital, Third Military Medical University, Chongqing, 400038, China. yupeiwu0l@sina.com.
Abstract

Adipocyte enhancer binding protein 1 (AEBP1) is a transcriptional repressor that plays a critical role in regulating adipogenesis. Recent studies have indicated that AEBP1 might function as a candidate oncogene and is overexpressed in several human malignancies. However, the role of AEBP1 in gastric Cancer (GC) remains largely unknown. This study aimed to investigate the expression pattern, prognostic significance and biological function of AEBP1 in human gastric Cancer and to explore the underlying mechanism. We found that both the mRNA and protein levels of AEBP1 were significantly increased in human GC tissues. Elevated AEBP1 expression was significantly correlated with poor overall survival in patients with both early-stage (Tumor, Node, Metastases (TNM) TNM I and II) and late-stage (TNM III and IV) GC. Silencing AEBP1 markedly suppressed the proliferation, migration, invasion, metastasis and epithelial-mesenchymal transition of GC cells. Moreover, we demonstrated that knockdown of AEBP1 in GC cells led to inhibition of the NF-κB pathway by hampering the degradation of IκBα. Thus, AEBP1 might be served as a promising prognostic indicator and a potential therapeutic target in human GC.

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