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

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)-IκB autocrine signaling. Drug treatments targeting CTGF, TNFR1, and IκB signaling each prohibited the EMT and tumor progression.
Authors	Xiaoping Zhu, Jing Zhong, Zhen Zhao, Jianting Sheng, Jiang Wang, Jiyong Liu, Kemi Cui, Jenny Chang, Hong Zhao, Stephen Wong
Journal	Oncotarget (Oncotarget) Vol. 6 Issue 28 Pg. 25320-38 (Sep 22 2015) ISSN: 1949-2553 [Electronic] United States
PMID	26318291 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
Chemical References	Antineoplastic Agents CCN2 protein, human Collagen Type I I-kappa B Proteins Receptors, Tumor Necrosis Factor, Type I TNFRSF1A protein, human Connective Tissue Growth Factor
Topics	Animals Antineoplastic Agents (pharmacology) Autocrine Communication Breast Neoplasms (genetics, metabolism, mortality, pathology, therapy) Cell Line, Tumor Cell Movement Cell Proliferation Collagen Type I (metabolism) Connective Tissue Growth Factor (antagonists & inhibitors, genetics, metabolism) Disease-Free Survival Epithelial Cells (drug effects, metabolism, pathology) Epithelial-Mesenchymal Transition Female Gene Expression Regulation, Neoplastic Humans I-kappa B Proteins (antagonists & inhibitors, metabolism) Kaplan-Meier Estimate Mice, Inbred BALB C Mice, Nude Neoplasm Invasiveness Neoplasm Metastasis RNA Interference Receptors, Tumor Necrosis Factor, Type I (antagonists & inhibitors, metabolism) Signal Transduction Stromal Cells (drug effects, metabolism, pathology) Time Factors Transfection Xenograft Model Antitumor Assays

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