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上皮来源的结缔组织生长因子通过诱导上皮-间质转化和I型胶原纤维沉积促进乳腺肿瘤进展。

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

作者信息

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

机构信息

Department of Systems Medicine and Bioengineering, Houston Methodist Research Institute, Weill Cornell Medical College, Houston, TX, USA.

Department of Radiology, The Teaching Hospital of Fujian Medical University, Fujian Provincial Cancer Hospital, Fuzhou, China.

出版信息

Oncotarget. 2015 Sep 22;6(28):25320-38. doi: 10.18632/oncotarget.4659.

DOI:10.18632/oncotarget.4659
PMID:26318291
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4694834/
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.

摘要

在肿瘤进展过程中，肿瘤细胞、基质细胞和细胞外基质成分之间的相互作用是通过细胞因子介导的。我们对已发表的临床乳腺癌队列中的132种已知细胞因子和生长因子以及我们的84个患者来源的异种移植模型进行分析后发现，肿瘤上皮细胞中结缔组织生长因子（CTGF）水平升高与不良的临床预后和结局显著相关。CTGF能够诱导肿瘤细胞上皮-间质转化（EMT），并促进I型胶原纤维的基质沉积，以刺激肿瘤生长和转移。这个过程是通过CTGF-肿瘤坏死因子受体I（TNFR1）-IκB自分泌信号介导的。针对CTGF、TNFR1和IκB信号的药物治疗均能抑制EMT和肿瘤进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6b4/4694834/3414b8dabfaa/oncotarget-06-25320-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6b4/4694834/606435f8fdd7/oncotarget-06-25320-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6b4/4694834/c643c27b2d90/oncotarget-06-25320-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6b4/4694834/4348263543a1/oncotarget-06-25320-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6b4/4694834/f7fa1ac6b8d6/oncotarget-06-25320-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6b4/4694834/f23d2e122ef5/oncotarget-06-25320-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6b4/4694834/2cca8fb9d1ed/oncotarget-06-25320-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6b4/4694834/5dbb546f6a61/oncotarget-06-25320-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6b4/4694834/cc49aaa5ce19/oncotarget-06-25320-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6b4/4694834/e6e54d4e6110/oncotarget-06-25320-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6b4/4694834/3414b8dabfaa/oncotarget-06-25320-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6b4/4694834/606435f8fdd7/oncotarget-06-25320-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6b4/4694834/c643c27b2d90/oncotarget-06-25320-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6b4/4694834/4348263543a1/oncotarget-06-25320-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6b4/4694834/f7fa1ac6b8d6/oncotarget-06-25320-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6b4/4694834/f23d2e122ef5/oncotarget-06-25320-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6b4/4694834/2cca8fb9d1ed/oncotarget-06-25320-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6b4/4694834/5dbb546f6a61/oncotarget-06-25320-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6b4/4694834/cc49aaa5ce19/oncotarget-06-25320-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6b4/4694834/e6e54d4e6110/oncotarget-06-25320-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6b4/4694834/3414b8dabfaa/oncotarget-06-25320-g010.jpg

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