Integrative characterisation of secreted factors involved in intercellular communication between prostate epithelial or cancer cells and fibroblasts

被引:7
|
作者
Wu, Yunjian [1 ,2 ]
Clark, Kimberley C. [1 ,2 ]
Niranjan, Birunthi [1 ,3 ]
Chueeh, Anderly C. [1 ,2 ]
Horvath, Lisa G. [4 ,5 ,6 ]
Taylor, Renea A. [1 ,7 ,8 ,9 ]
Daly, Roger J. [1 ,9 ]
机构
[1] Monash Univ, Biomed Discovery Inst, Canc Program, Clayton, Vic, Australia
[2] Monash Univ, Dept Biochem & Mol Biol, Clayton, Vic, Australia
[3] Monash Univ, Dept Anat & Dev Biol, Clayton, Vic, Australia
[4] Garvan Inst Med Res, Darlinghurst, NSW, Australia
[5] Univ Sydney, Sydney, NSW, Australia
[6] Chris OBrien Lifehouse, Sydney, NSW, Australia
[7] Monash Univ, Dept Physiol, Clayton, Vic, Australia
[8] Univ Melbourne, Peter MacCallum Canc Ctr, Canc Res Div, Melbourne, Vic, Australia
[9] Monash Univ, Biomed Discovery Inst, Canc Program, Clayton, Vic 3800, Australia
基金
澳大利亚国家健康与医学研究理事会;
关键词
cell signalling; chemokine; co-culture; cytokine; follistatin; tumour microenvironment; MESENCHYMAL TRANSITION; ANTIANDROGEN RESISTANCE; SERUM FOLLISTATIN; ACTIVIN-A; TGF-ALPHA; TUMOR; RECEPTOR; MICROENVIRONMENT; PROLIFERATION; PROGRESSION;
D O I
10.1002/1878-0261.13376
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Reciprocal interactions between prostate cancer cells and carcinoma-associated fibroblasts (CAFs) mediate cancer development and progression; however, our understanding of the signalling pathways mediating these cellular interactions remains incomplete. To address this, we defined secretome changes upon co-culture of prostate epithelial or cancer cells with fibroblasts that mimic bi-directional communication in tumours. Using antibody arrays, we profiled conditioned media from mono- and co-cultures of prostate fibroblasts, epithelial and cancer cells, identifying secreted proteins that are upregulated in co-culture compared to mono-culture. Six of these (CXCL10, CXCL16, CXCL6, FST, PDGFAA, IL-17B) were functionally screened by siRNA knockdown in prostate cancer cell/fibroblast co-cultures, revealing a key role for follistatin (FST), a secreted glycoprotein that binds and bioneutralises specific members of the TGF-beta superfamily, including activin A. Expression of FST by both cell types was required for the fibroblasts to enhance prostate cancer cell proliferation and migration, whereas FST knockdown in co-culture grafts decreased tumour growth in mouse xenografts. This study highlights the complexity of prostate cancer cell-fibroblast communication, demonstrates that co-culture secretomes cannot be predicted from individual cultures, and identifies FST as a tumour-microenvironment-derived secreted factor that represents a candidate therapeutic target.
引用
收藏
页码:469 / 486
页数:18
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