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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Meng, Mingyao Wang, Wenju Yan, Jun Tan, Jing Liao, Liwei Shi, Jianlin Wei, Chuanyu Xie, Yanhua Jin, Xingfang Yang, Li Jin, Qing Zhu, Huirong Tan, Weiwei Yang, Fang Hou, Zongliu |
| Description | Author Affiliation: Meng M ( Department of Central Laboratory, Yan'an Affiliated Hospital of Kunming Medical University, No. 245 East of Renmin Road, Kunming, 650051, Yunnan, People's Republic of China.); Wang W ( Yunnan Cell Biology and Clinical Translation Research Center, Kunming, 650051, Yunnan, People's Republic of China.); Yan J ( Department of Central Laboratory, Yan'an Affiliated Hospital of Kunming Medical University, No. 245 East of Renmin Road, Kunming, 650051, Yunnan, People's Republic of China.); Tan J ( Yunnan Cell Biology and Clinical Translation Research Center, Kunming, 650051, Yunnan, People's Republic of China.); Liao L ( Department of Central Laboratory, Yan'an Affiliated Hospital of Kunming Medical University, No. 245 East of Renmin Road, Kunming, 650051, Yunnan, People's Republic of China.); Shi J ( Department of Central Laboratory, Yan'an Affiliated Hospital of Kunming Medical University, No. 245 East of Renmin Road, Kunming, 650051, Yunnan, People's Republic of China.); Wei C ( Department of Central Laboratory, Yan'an Affiliated Hospital of Kunming Medical University, No. 245 East of Renmin Road, Kunming, 650051, Yunnan, People's Republic of China.); Xie Y ( Department of Central Laboratory, Yan'an Affiliated Hospital of Kunming Medical University, No. 245 East of Renmin Road, Kunming, 650051, Yunnan, People's Republic of China.); Jin X ( Yunnan Cell Biology and Clinical Translation Research Center, Kunming, 650051, Yunnan, People's Republic of China.); Yang L ( Department of Central Laboratory, Yan'an Affiliated Hospital of Kunming Medical University, No. 245 East of Renmin Road, Kunming, 650051, Yunnan, People's Republic of China.); Jin Q ( Yunnan Cell Biology and Clinical Translation Research Center, Kunming, 650051, Yunnan, People's Republic of China.); Zhu H ( Department of Central Laboratory, Yan'an Affiliated Hospital of Kunming Medical University, No. 245 East of Renmin Road, Kunming, 650051, Yunnan, People's Republic of China.); Tan W ( Yunnan Cell Biology and Clinical Translation Research Center, Kunming, 650051, Yunnan, People's Republic of China.); Yang F ( Department of Central Laboratory, Yan'an Affiliated Hospital of Kunming Medical University, No. 245 East of Renmin Road, Kunming, 650051, Yunnan, People's Republic of China.); Hou Z ( Yunnan Cell Biology and Clinical Translation Research Center, Kunming, 650051, Yunnan, People's Republic of China.) |
| Abstract | Unlike heterogeneous tumor cells, cancer-associated fibroblasts (CAF) are genetically more stable which serve as a reliable target for tumor immunotherapy. Fibroblast activation protein (FAP) which is restrictively expressed in tumor cells and CAF in vivo and plays a prominent role in tumor initiation, progression, and metastasis can function as a tumor rejection antigen. In the current study, we have constructed artificial FAP(+) stromal cells which mimicked the FAP(+) CAF in vivo. We immunized a breast cancer mouse model with FAP(+) stromal cells to perform immunotherapy against FAP(+) cells in the tumor microenvironment. By forced expression of FAP, we have obtained FAP(+) stromal cells whose phenotype was CD11b(+)/CD34(+)/Sca-1(+)/FSP-1(+)/MHC class I(+). Interestingly, proliferation capacity of the fibroblasts was significantly enhanced by FAP. In the breast cancer-bearing mouse model, vaccination with FAP(+) stromal cells has significantly inhibited the growth of allograft tumor and reduced lung metastasis indeed. Depletion of T cell assays has suggested that both CD4(+) and CD8(+) T cells were involved in the tumor cytotoxic immune response. Furthermore, tumor tissue from FAP-immunized mice revealed that targeting FAP(+) CAF has induced apoptosis and decreased collagen type I and CD31 expression in the tumor microenvironment. These results implicated that immunization with FAP(+) stromal cells led to the disruption of the tumor microenvironment. Our study may provide a novel strategy for immunotherapy of a broad range of cancer. |
| File Format | HTM / HTML |
| ISSN | 10104283 |
| Issue Number | 8 |
| Journal | Tumor Biology |
| Volume Number | 37 |
| e-ISSN | 14230380 |
| Language | English |
| Publisher | Springer |
| Publisher Date | 2016-08-01 |
| Publisher Place | Netherlands |
| Access Restriction | Subscribed |
| Content Type | Text |
| Resource Type | Article |
| Subject | Medicine Cancer Research |
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