ESE3 inhibits pancreatic cancer metastasis by upregulating E-cadherin

Tiansuo Zhao, Wenna Jiang, Xiuchao Wang, Hongwei Wang, Chen Zheng, Yang Li, Yan Sun, Chongbiao Huang, Zhi Bo Han, Shengyu Yang, Zhiliang Jia, Keping Xie, He Ren, Jihui Hao

Research output: Contribution to journalArticlepeer-review

43 Scopus citations


The ETS family transcription factor ESE3 is a crucial element in differentiation and development programs for many epithelial tissues. Here we report its role as a tumor suppressor in pancreatic cancer. We observed drastically lower ESE3 expression in pancreatic ductal adenocarcinomas (PDAC) compared with adjacent normal pancreatic tissue. Reduced expression of ESE3 in PDAC correlated closely with an increase in lymph node metastasis and vessel invasion and a decrease in relapsefree and overall survival in patients. In functional experiments, downregulating the expression of ESE3 promoted PDAC cell motility and invasiveness along with metastasis in an orthotopic mouse model. Mechanistic studies in PDAC cell lines, the orthotopic mouse model, and human PDAC specimens demonstrated that ESE3 inhibited PDAC metastasis by directly upregulating E-cadherin expression at the level of its transcription. Collectively, our results establish ESE3 as a negative regulator of PDAC progression and metastasis by enforcing E-cadherin upregulation.

Original languageEnglish (US)
Pages (from-to)874-885
Number of pages12
JournalCancer Research
Issue number4
StatePublished - Feb 15 2017

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research


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