Epithelial derived CTGF promotes breast tumor progression via inducing EMT and collagen I fibers deposition

Xiaoping Zhu, Jing Zhong, Zhen Zhao, Jianting Sheng, Jiang Wang, Jiyong Liu, Kemi Cui, Jenny Chang, Hong Zhao, Stephen Wong

Research output: Contribution to journalArticlepeer-review

22 Scopus citations

Abstract

Interactions among tumor cells, stromal cells, and extracellular matrix compositions are mediated through cytokines during tumor progression. Our analysis of 132 known cytokines and growth factors in published clinical breast cohorts and our 84 patient-derived xenograft models revealed that the elevated connective tissue growth factor (CTGF) in tumor epithelial cells significantly correlated with poor clinical prognosis and outcomes. CTGF was able to induce tumor cell epithelial-mesenchymal transition (EMT), and promote stroma deposition of collagen I fibers to stimulate tumor growth and metastasis. This process was mediated through CTGF-tumor necrosis factor receptor I (TNFR1)-I?B autocrine signaling. Drug treatments targeting CTGF, TNFR1, and I?B signaling each prohibited the EMT and tumor progression.

Original languageEnglish (US)
Pages (from-to)25320-25338
Number of pages19
JournalOncotarget
Volume6
Issue number28
DOIs
StatePublished - 2015

Keywords

  • Epithelial-mesenchymal transition (EMT)
  • breast cancer
  • collagen I fibers
  • connective tissue growth factor (CTGF)
  • tumor necrosis factor receptor 1 (TNFR1) pathway

ASJC Scopus subject areas

  • Oncology

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