Research Papers:

New therapy with ASC-J9® to suppress the prostatitis via altering the cytokine CCL2 signals

Shin-Jen Lin, Fu-Ju Chou, Chang-Yi Lin, Hong-Chiang Chang, Shuyuan Yeh and Chawnshang Chang _

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Oncotarget. 2016; 7:66769-66775. https://doi.org/10.18632/oncotarget.11484

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Shin-Jen Lin1, Fu-Ju Chou1, Chang-Yi Lin1, Hong-Chiang Chang1, Shuyuan Yeh1, Chawnshang Chang1,2

1George Whipple Laboratory for Cancer Research, Departments of Pathology, Urology, and Radiation Oncology, and Wilmot Cancer Center, University of Rochester Medical Center, Rochester, NY 14642, USA

2Sex Hormone Research Center, China Medical University/Hospital, Taichung 404, Taiwan

Correspondence to:

Chawnshang Chang, email: [email protected]

Keywords: prostate, ASC-J9®, CCL2

Received: March 23, 2016     Accepted: July 19, 2016     Published: August 22, 2016


Prostatitis is a common disease contributing to 8% of all urologist visits. Yet the etiology and effective treatment remain to be further elucidated. Using a non-obese diabetes mouse model that can be induced by autoimmune response for the spontaneous development of prostatitis, we found that injection of the ASC-J9® at 75 mg/Kg body weight/48 hours led to significantly suppressed prostatitis that was accompanied with reduction of lymphocyte infiltration with reduced CD4+ T cells in prostate. In vitro studies with a co-culture system also confirmed that ASC-J9® treatment could suppress the CD4+ T cell migration to prostate stromal cells. Mechanisms dissection indicated that ASC-J9® can suppress CD4+ T cell migration via decreasing the cytokine CCL2 in vitro and in vivo, and restoring CCL2 could interrupt the ASC-J9® suppressed CD4+ T cell migration. Together, results from in vivo and in vitro studies suggest that ASC-J9® can suppress prostatitis by altering the autoimmune response induced by CD4+ T cell recruitment, and using ASC-J9® may help us to develop a potential new therapy to battle the prostatitis with little side effects.

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