scholarly journals Lobe-Specific Carcinogenesis in the Transgenic Adenocarcinoma of Mouse Prostate (TRAMP) Mouse Model

10.5772/54904 ◽  
2013 ◽  
Author(s):  
Jinhui Zhang ◽  
Lei Wang ◽  
Yong Zhang ◽  
Junxuan Lu
Keyword(s):  
Mouse Model ◽  
Tramp Mouse ◽  
Mouse Prostate

scholarly journals Endocytic Adaptor Protein Epsin Is Elevated in Prostate Cancer and Required for Cancer Progression

ISRN Oncology ◽  
2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Kandice L. Tessneer ◽  
Satish Pasula ◽  
Xiaofeng Cai ◽  
Yunzhou Dong ◽  
Xiaolei Liu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Mouse Model ◽  
Cancer Cells ◽  
Potential Role ◽  
Adaptor Protein ◽  
Wild Type ◽  
Prostate Cancer Cells ◽  
Prostate Tumorigenesis ◽  
Tramp Mouse ◽  
Mouse Prostate

Epsins have an important role in mediating clathrin-mediated endocytosis of ubiquitinated cell surface receptors. The potential role for epsins in tumorigenesis and cancer metastasis by regulating intracellular signaling pathways has largely not been explored. Epsins are reportedly upregulated in several types of cancer including human skin, lung, and canine mammary cancers. However, whether their expression is elevated in prostate cancer is unknown. In this study, we investigated the potential role of epsins in prostate tumorigenesis using the wild type or epsin-deficient human prostate cancer cells, LNCaP, in a human xenograft model, and the spontaneous TRAMP mouse model in wild type or epsin-deficient background. Here, we reported that the expression of epsins 1 and 2 is upregulated in both human and mouse prostate cancer cells and cancerous tissues. Consistent with upregulation of epsins in prostate tumors, we discovered that depletion of epsins impaired tumor growth in both the human LNCaP xenograft and the TRAMP mouse prostate. Furthermore, epsin depletion significantly prolonged survival in the TRAMP mouse model. In summary, our findings suggest that epsins may act as oncogenic proteins to promote prostate tumorigenesis and that depletion or inhibition of epsins may provide a novel therapeutic target for future prostate cancer therapies.

Role of GM-CSF in a mouse model of experimental autoimmune prostatitis

2019 ◽  
Vol 317 (1) ◽  
pp. F23-F29 ◽  
Author(s):  
Yaxiao Liu ◽  
Yan Li ◽  
Qinggang Liu ◽  
Zonglong Wu ◽  
Jianfeng Cui ◽  
...  
Keyword(s):  
Mouse Model ◽  
Dorsal Root Ganglia ◽  
Knockout Mice ◽  
Dorsal Root ◽  
Prostate Tissue ◽  
Mrna Levels ◽  
Gm Csf ◽  
Mouse Prostate ◽  
Experimental Autoimmune

The etiology of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is still unknown. Granulocyte macrophage colony-stimulating factor (GM-CSF) has been shown to play an important role in the development of autoimmune and inflammatory diseases. Here, we investigated the expression and function of GM-CSF in patients with CP/CPPS and in a mouse model of experimental autoimmune prostatitis (EAP). GM-CSF mRNA levels were detected in expressed prostatic secretions samples from patients with CP/CPPS and in prostate tissue from a mouse model of EAP. The expression of GM-CSF receptor in mouse prostate and dorsal root ganglia were determined using PCR and immunohistochemistry. Behavioral testing and inflammation scoring were performed to evaluate the role of GM-CSF in disease development and symptom severity of EAP using GM-CSF knockout mice. mRNA levels of putative nociceptive and inflammatory markers were measured in the prostate after the induction of EAP. Elevated GM-CSF mRNA levels were observed in expressed prostatic secretions samples from patients with CP/CPPS compared with healthy volunteers. GM-CSF mRNA was also significantly increased in prostate tissue of the EAP mice model. The expression of GM-CSF receptors was confirmed in mouse prostate and dorsal root ganglia. GM-CSF knockout mice showed fewer Infiltrating leukocytes and pain symptoms after the induction of EAP. Deletion of GM-CSF significantly diminished EAP-induced increases of chemokine (C-C motif) ligand 2, chemokine (C-C motif) ligand 3, and nerve growth factor mRNA expression. The results indicated that GM-CSF plays a functional role in the pathogenesis of EAP. GM-CSF may function as a signaling mediator for both inflammation and pain transduction in CP/CPPS.

scholarly journals X-linked inhibitor of apoptosis deficiency in the TRAMP mouse prostate cancer model

2008 ◽  
Vol 15 (5) ◽  
pp. 831-840 ◽  
Author(s):  
C Hwang ◽  
K A Oetjen ◽  
D Kosoff ◽  
K J Wojno ◽  
M A Albertelli ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Inhibitor Of Apoptosis ◽  
Cancer Model ◽  
Tramp Mouse ◽  
Mouse Prostate ◽  
Prostate Cancer Model

scholarly journals Dysfunctional Transforming Growth Factor-β Receptor II Accelerates Prostate Tumorigenesis in the TRAMP Mouse Model

2009 ◽  
Vol 69 (18) ◽  
pp. 7366-7374 ◽  
Author(s):  
Hong Pu ◽  
Joanne Collazo ◽  
Elisabeth Jones ◽  
Dustin Gayheart ◽  
Shinichi Sakamoto ◽  
...  
Keyword(s):  
Growth Factor ◽  
Mouse Model ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Prostate Tumorigenesis ◽  
Tramp Mouse ◽  
Β Receptor

scholarly journals Prevention of Prostate Cancer with Oleanane Synthetic Triterpenoid CDDO-Me in the TRAMP Mouse Model of Prostate Cancer

Cancers ◽  
2011 ◽  
Vol 3 (3) ◽  
pp. 3353-3369 ◽  
Author(s):  
Xiaohua Gao ◽  
Dorrah Deeb ◽  
Yongbo Liu ◽  
Ali S. Arbab ◽  
George W. Divine ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Mouse Model ◽  
Tramp Mouse

scholarly journals Transgenic overexpression of NanogP8 in the mouse prostate is insufficient to initiate tumorigenesis but weakly promotes tumor development in the Hi-Myc mouse model

Oncotarget ◽  
2017 ◽  
Vol 8 (32) ◽  
pp. 52746-52760
Author(s):  
Bigang Liu ◽  
Shuai Gong ◽  
Qiuhui Li ◽  
Xin Chen ◽  
John Moore ◽  
...  
Keyword(s):  
Mouse Model ◽  
Tumor Development ◽  
Mouse Prostate

244: The Aflavins Inhibit Prostate Carcinogenesis in the TRAMP Mouse Model

2006 ◽  
Vol 175 (4S) ◽  
pp. 81-81
Author(s):  
James Thorpe ◽  
Sunjay Jain ◽  
Timothy Marczylo ◽  
Andreas Gescher ◽  
William Steward ◽  
...  
Keyword(s):  
Mouse Model ◽  
Tramp Mouse ◽  
Prostate Carcinogenesis
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