Identification of genes potentially involved in the acquisition of androgen-independent and metastatic tumor growth in an autochthonous genetically engineered mouse prostate cancer model

The Prostate ◽  
2006 ◽  
Vol 67 (1) ◽  
pp. 83-106 ◽  
Author(s):  
Sharon D. Morgenbesser ◽  
Rajashree P. McLaren ◽  
Brenda Richards ◽  
Mindy Zhang ◽  
Viatcheslav R. Akmaev ◽  
...  
2009 ◽  
Vol 8 (4) ◽  
pp. 7290.2009.00020 ◽  
Author(s):  
Jim W. Xuan ◽  
Michael Bygrave ◽  
Fatma Valiyeva ◽  
Madeleine Moussa ◽  
Jonathan I. Izawa ◽  
...  

1996 ◽  
Vol 24 (4) ◽  
pp. 502-504 ◽  
Author(s):  
J.R. Gingrich ◽  
N.M. Greenberg

2005 ◽  
Vol 13 (1) ◽  
pp. 91-98 ◽  
Author(s):  
T Saika ◽  
N Kusaka ◽  
V Mouraviev ◽  
T Satoh ◽  
H Kumon ◽  
...  

Biology ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 67 ◽  
Author(s):  
Yu-Ching Fan ◽  
Wei-Yu Chen ◽  
Kuan-Der Lee ◽  
Yuan-Chin Tsai

Background: Several lines of evidence have demonstrated the tumor-promoting function of inflammation. Since many chemokines are important in coordinating immune cells during inflammation, monitoring intratumoral chemokines provides a way to study the tumor microenvironment. Methods: To identify tumorigenic chemokines, we compared two syngeneic mouse prostate cancer cell lines by an antibody array and quantitative reverse-transcription polymerase chain reaction (RT-PCR). The tumor microenvironment was analyzed by monitoring gene expressions in mouse tumor tissues, primary cells, and tumor-infiltrating leukocytes (TILs). Result: We identified a group of pro-inflammatory chemokines associated with a tumorigenic transgenic adenocarcinoma mouse prostate (TRAMP)-C1 cell line. In the tumor microenvironment, the TILs secrete a natural anti-inflammatory factor, interleukin-1 receptor antagonist (IL1RN), which inhibits the functions of pro-inflammatory molecules and likely accounts for tumor type-specific anti-inflammation functions. Conclusion: Our results support that tumor cells recruit TILs by pro-inflammatory chemokines to establish an IL1RN-mediated anti-inflammatory environment in the syngeneic prostate cancer model.


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