Journal
ONCOIMMUNOLOGY
Volume 5, Issue 11, Pages -Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/2162402X.2016.1234570
Keywords
BMP4; EMT; immunotherapy; lung cancer; miR-200; PD-L1
Categories
Funding
- Uniting Against Lung Cancer/Lung Cancer Research Foundation award
- Rexanna's Foundation for Fighting Lung Cancer
- ACS RSG [LIB-117155, 5-P50-CA70907-12 PP-3b]
- CPRIT Graduate Scholar Training Grant [RP140106]
- NIH Cancer Center Support Grant [CA016672]
- Jeane F. Shelby Scholarship Fund
- CPRIT [RP150405]
- [2P50CA070907-16A1]
- [NRF-2014R1A1A1002340]
- [2010-0027945]
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Cancer cells modulate the recruitment and function of inflammatory cells to create an immunosuppressive microenvironment that favors tumor growth and metastasis. However, the tumor-derived regulatory programs that promote intratumoral immunosuppression remain poorly defined. Here, we show in a Kras(LA1/+)p53(R172H Delta g/+)-based mouse model that bone morphogenetic protein-4 (BMP4) augments the expression of the T cell co-inhibitory receptor ligand PD-L1 in the mesenchymal subset of lung cancer cells, leading to profound CD8(+) T cell-mediated immunosuppression, producing tumor growth and metastasis. We previously reported in this model that BMP4 functions as a pro-tumorigenic factor regulated by miR-200 via GATA4/6. Thus, BMP4-mediated immunosuppression is part of a larger miR-200-directed gene expression program in tumors that promotes tumor progression, which could have important implications for cancer treatment.
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